Increased Total Eosinophil Count
An increased total eosinophil count, also known as eosinophilia, refers to a higher than normal number of eosinophils circulating in the blood. Eosinophils are a type of white blood cell, or leukocyte, that plays a specialized role in the body’s immune system.
Eosinophils originate and mature in the bone marrow before entering the bloodstream. Their primary biological function involves defending the body against parasitic infections and modulating allergic and inflammatory responses. They contain granules filled with various proteins and enzymes that are released upon activation, contributing to tissue inflammation and pathogen destruction.
Clinically, an elevated eosinophil count is a common finding and can be indicative of several underlying conditions. The most frequent causes include allergic diseases such as asthma, allergic rhinitis, eczema, and drug hypersensitivity reactions. Parasitic infections are another significant cause of eosinophilia. Less commonly, it can be associated with certain autoimmune disorders, some cancers (particularly hematologic malignancies), and rare primary eosinophilic disorders. The measurement of eosinophil counts is a standard component of a complete blood count (CBC) and is routinely used as a diagnostic and monitoring tool in clinical practice. Genetic studies have identified specific loci associated with eosinophil counts, includingrs4328821 in the GATA2 locus, rs2516399 in the MHC region, and rs9373124 in the HBS1L-MYB locus [1]. Research efforts continue to identify multiple genetic loci influencing various white blood cell phenotypes, including those related to eosinophil counts[1].
The social importance of understanding and managing increased eosinophil counts is substantial, particularly due to the high prevalence of allergic diseases and asthma worldwide. Eosinophilia can contribute to the severity and chronicity of these conditions, impacting quality of life and healthcare burdens. Monitoring eosinophil levels helps healthcare providers diagnose, assess disease activity, and guide treatment strategies, including the use of targeted therapies that reduce eosinophil numbers. Further genetic research into the factors influencing eosinophil counts contributes to a deeper understanding of immune regulation and genetic predispositions to common inflammatory and allergic diseases.
Limitations
Section titled “Limitations”Understanding the genetic underpinnings of increased total eosinophil count presents several challenges and limitations that warrant careful consideration when interpreting research findings. These limitations span methodological aspects, generalizability across diverse populations, and the intricate interplay with environmental factors.
Methodological and Statistical Considerations
Section titled “Methodological and Statistical Considerations”Current genetic studies, particularly genome-wide association studies (GWAS), often involve large sample sizes, yet these may still be insufficient to detect all genetic variants contributing to increased total eosinophil count, especially those with rare frequencies or very small effect sizes (Reiner AP, 2011; Crosslin DR, 2011). The stringent statistical thresholds required for genome-wide significance can lead to weak individual genetic associations, where many genes show suggestive rather than definitively significant signals, making robust replication challenging (Cusanovich DA, 2012). Indeed, some identified associations have remained inconclusive after initial in silico testing, necessitating further direct genotyping to confirm their relevance (van der Harst P, 2012). While some loci are consistently replicated across studies, the frequent discovery of novel associations highlights the complex and still incompletely mapped genetic architecture of eosinophil count (Okada Y, 2011).
Population Diversity and Phenotype Assessment
Section titled “Population Diversity and Phenotype Assessment”A significant limitation arises from the population-specific nature of many genetic studies. Research often focuses on particular ancestral groups, such as African Americans, individuals from isolated founder populations like Kosrae or Korcula Island, or specific ethnic groups like Japanese or Hispanic children (Reiner AP, 2011; Lowe JK, 2009; Zemunik T, 2009; Okada Y, 2011; Comuzzie AG, 2012). While providing valuable insights into these populations, the findings may not be directly generalizable to other global populations, potentially missing important ancestry-specific genetic variants or variations in effect sizes. Furthermore, the accuracy and consistency of phenotype assessment are critical. Eosinophil counts are typically determined from peripheral blood samples, but confounding factors such as the use of medications like antibiotics or steroids at the time of collection can influence results (Cusanovich DA, 2012). Differences in the timing of blood sample collection, sometimes spanning several years, can also introduce variability, despite efforts to adjust for known factors like age, sex, and time of day (Ferreira MA, 2009; Cusanovich DA, 2012).
Environmental and Gene-Environment Interactions
Section titled “Environmental and Gene-Environment Interactions”Eosinophil count is highly sensitive to a myriad of environmental and physiological factors, including allergic exposures, parasitic infections, and various health conditions. While genetic studies typically adjust for basic demographic variables, fully elucidating the complex interplay between these environmental factors and genetic predispositions is a formidable task that is often not comprehensively captured (Cusanovich DA, 2012). This incomplete accounting for environmental influences contributes to the phenomenon of “missing heritability,” where a substantial portion of the genetic variance for increased total eosinophil count remains unexplained by identified common genetic variants. Current research primarily focuses on common variants with small individual effects, leaving a significant gap in understanding the contributions of rare variants, structural genomic variations, and intricate gene-gene or gene-environment interactions, which likely play a crucial role in the overall variability of eosinophil counts.
Variants
Section titled “Variants”Genetic variations play a crucial role in influencing an individual’s total eosinophil count, a key indicator in immune and inflammatory responses. While many factors contribute to eosinophil levels, specific single nucleotide polymorphisms (SNPs) within or near genes can alter their function, thereby impacting the production, differentiation, or activity of these white blood cells. Genome-wide association studies have identified several genetic loci associated with white blood cell subtypes, including eosinophils, underscoring the genetic architecture underlying these hematological traits[1].
Variants like rs548473684 in the ETNPPL gene, rs182216696 near GUCY1B1, and rs184350460 in CHRNA7exemplify genes with diverse cellular roles that can indirectly influence eosinophil dynamics.ETNPPL(Ethanolamine-phosphate phospho-lyase) is involved in phospholipid metabolism, a fundamental process for maintaining cell membrane integrity and regulating cell signaling pathways, which are critical for immune cell function. Alterations inETNPPLactivity could affect the lipid environment essential for eosinophil development or their response to inflammatory signals.GUCY1B1 encodes a subunit of soluble guanylate cyclase, an enzyme responsible for producing cyclic GMP (cGMP), a vital second messenger. cGMP signaling modulates various physiological processes, including immune cell activation and inflammatory responses, suggesting that a variant in GUCY1B1could impact eosinophil behavior by altering cGMP levels. Furthermore,CHRNA7codes for a subunit of the nicotinic acetylcholine receptor, which is part of the cholinergic anti-inflammatory pathway; this pathway helps to regulate immune responses, and its dysregulation could contribute to heightened inflammation and elevated eosinophil counts[2]. Such sequence variants affecting eosinophil numbers have been associated with conditions like asthma and myocardial infarction[3].
Other variants, such as rs535927353 near ZNF24TR, rs555966576 within the NOS2 - LYRM9 region, and rs567360199 associated with ASB6 - PRRX2, highlight genes involved in gene regulation, metabolism, and protein degradation. ZNF24 (Zinc Finger Protein 24) is a transcription factor that regulates the expression of other genes, and a variant in its transcriptional regulator region could broadly influence cellular processes, including those in hematopoietic stem cells that give rise to eosinophils. NOS2(Nitric Oxide Synthase 2) produces nitric oxide (NO), a crucial signaling molecule in inflammation, and variations affecting its activity could alter local NO concentrations, influencing eosinophil survival and activation.LYRM9 is involved in mitochondrial complex I assembly, impacting cellular energy production, which is vital for the metabolic demands of active immune cells like eosinophils. Additionally, ASB6(Ankyrin Repeat And SOCS Box Containing 6) is part of a family of proteins that regulate cytokine signaling, whilePRRX2(Paired Related Homeobox 2) is a transcription factor involved in cell differentiation and development. Variants in these genes could therefore modulate the intricate pathways that control eosinophil production, maturation, and their contribution to inflammatory states[4].
Long non-coding RNAs (lncRNAs) and pseudogenes also represent regions where genetic variants can exert influence. Variants like rs568375457 in LINC00581, rs150833850 near LINC02648 - LINP1, and rs182666451 associated with RNA5SP267 - SLC2A13P1 involve non-coding elements. LncRNAs such as LINC00581, LINC02648, and LINP1 are increasingly recognized for their roles in regulating gene expression, affecting processes from chromatin modification to mRNA stability, which can indirectly impact immune cell biology. Pseudogenes, like RNA5SP267 and SLC2A13P1, though often non-functional copies of genes, can sometimes have regulatory roles, influencing the expression of their functional counterparts or acting as competing endogenous RNAs. Finally, rs548300984 , located near GRIN2B - MRPS18CP4, involves GRIN2B, a subunit of the NMDA receptor primarily known for neuronal function, but with emerging evidence of wider roles, and MRPS18CP4, a pseudogene. The collective impact of such variants across the genome can explain a significant portion of the variation observed in white blood cell subtypes, influencing up to 2.1% of the variations in the counts of white blood cell subtypes [1].
Key Variants
Section titled “Key Variants”Definition and Measurement of Eosinophil Count
Section titled “Definition and Measurement of Eosinophil Count”An increased total eosinophil count refers to an elevated number of eosinophils, a specific type of white blood cell, found in peripheral blood. Eosinophil counts are quantitatively determined as part of a differential blood count, a standard laboratory procedure used to assess various white blood cell subtypes[5]. The results are typically reported in absolute numbers, such as thousands of cells per milliliter of blood, or as a percentage of the total white blood cell count [2]. While specific diagnostic thresholds for an “increased” count can vary, studies often report median values or ranges, for instance, median eosinophil percentages ranging from 1.3% to 3.2% in different populations[6].
Classification and Nomenclature of Eosinophils
Section titled “Classification and Nomenclature of Eosinophils”Eosinophils are classified as one of the five major subtypes of white blood cells, alongside neutrophils, monocytes, basophils, and lymphocytes [1]. The terminology “eosinophil count” is a precise and widely accepted term, reflecting the quantitative assessment of these cells. The study of eosinophil counts often employs a dimensional approach, treating the count as a continuous quantitative trait rather than a purely categorical disease state, particularly in genetic research[1]. This approach allows for the identification of genetic loci that influence the variability of these counts within a population.
Genetic Determinants of Eosinophil Count
Section titled “Genetic Determinants of Eosinophil Count”Research into white blood cell subtypes has identified genetic loci significantly associated with eosinophil counts, highlighting a genetic basis for their regulation. For instance, specific genetic loci, including IL1RL1, IKZF2, and HBS1L-MYB, have been linked to eosinophil counts[1]. Furthermore, studies have shown that some genetic loci can be shared across different white blood cell subtypes, with one locus identified as being associated with both basophil and eosinophil counts[1]. These findings contribute to understanding the complex genetic architecture underlying hematopoiesis and the regulation of immune cell populations.
Causes of Increased Total Eosinophil Count
Section titled “Causes of Increased Total Eosinophil Count”Genetic Predisposition
Section titled “Genetic Predisposition”Variations in an individual’s genetic makeup play a significant role in influencing total eosinophil count. Genome-wide association studies (GWAS) have identified specific genetic loci associated with eosinophil levels, indicating a polygenic architecture where multiple inherited variants contribute to the trait. For instance, research conducted in a Japanese population identified three distinct loci significantly associated with eosinophil counts, including single nucleotide polymorphisms (SNPs) in theGATA2 locus (rs4328821 ), the Major Histocompatibility Complex (MHC) region (rs2516399 ), and the HBS1L-MYB locus (rs9373124 ) [1]. These findings suggest that genetic differences in genes involved in immune regulation and hematopoietic development can modulate the production and maintenance of eosinophils, thereby contributing to variations in their circulating numbers [1].
Further studies highlight the complexity and potential population-specific nature of these genetic influences. While certain genetic regions, such as the GATA2locus, were also found to be associated with basophil counts, suggesting common regulatory pathways for these granulocytes, other large-scale investigations did not identify genome-wide significant associations for eosinophil count[1]. This contrast underscores that the genetic landscape influencing eosinophil levels can vary across different ethnic groups or study designs, and that some genetic factors may exert subtle effects that require specific population contexts or larger cohorts for detection. The identified loci are thought to affect hematopoiesis, the process of blood cell formation, thereby influencing the differentiation, proliferation, or survival of eosinophilic granulocytes[1].
Eosinophil Biology and Hematopoiesis
Section titled “Eosinophil Biology and Hematopoiesis”Eosinophils are a specialized type of white blood cell, also known as leukocytes, which are integral components of the immune system. Their primary functions include defense against parasitic infections and modulation of allergic inflammatory responses. The development of eosinophils, like all blood cells, begins in the bone marrow from hematopoietic stem cells through a complex process called hematopoiesis[1]. This process involves a series of differentiation steps, where committed progenitor cells mature into eosinophils before circulating in the peripheral blood. The total eosinophil count observed in the bloodstream is a dynamic measure, reflecting the intricate balance between their production, survival, and egress into various tissues.
Genetic Determinants of Eosinophil Levels
Section titled “Genetic Determinants of Eosinophil Levels”The total eosinophil count in an individual is significantly influenced by genetic factors, with specific regions of the genome identified as contributing to variations in these cell numbers. Research has revealed several genetic loci associated with eosinophil counts, with three distinct loci identified in a Japanese population[1]. These include single nucleotide polymorphisms (SNPs) located within or in close proximity to theGATA2 gene, the Major Histocompatibility Complex (MHC) region, and the HBS1L-MYB locus [1]. These genetic findings underscore the role of inherited variations in modulating the complex biological processes that regulate eosinophil production and overall levels.
Further investigation into these genetic influences indicates that some loci may exert pleiotropic effects, impacting more than one type of white blood cell. For instance, one genetic locus has been identified as being shared between both basophil and eosinophil counts[1]. This shared genetic control points towards common regulatory pathways or progenitor cell origins that are critical for the development of these granulocyte lineages. Such interconnectedness highlights the intricate and shared functional roles of specific genetic variants within the broader context of hematopoiesis [1].
Molecular Pathways and Cellular Regulation
Section titled “Molecular Pathways and Cellular Regulation”The genes located within the identified loci for eosinophil counts are involved in fundamental molecular and cellular pathways essential for hematopoiesis and immune function. TheGATA2 gene, for example, encodes a crucial transcription factor, GATA2, which is indispensable for the development and maintenance of hematopoietic stem cells and various myeloid cell lineages, including eosinophils [1]. Therefore, genetic variations within GATA2can directly impact the regulatory networks that govern the proliferation and differentiation of eosinophil precursors, thereby influencing their numbers.
The MHC region, a highly polymorphic gene cluster, is widely recognized for its pivotal role in adaptive immunity, particularly in antigen presentation [1]. Beyond its direct immune functions, the MHC region also harbors genes that influence the development and regulation of immune cells. Genetic variants in this region could affect critical signaling pathways that control the maturation, survival, or function of eosinophils. Similarly, the HBS1L-MYB locus includes MYB, another transcription factor with a significant role in the proliferation and differentiation of hematopoietic cells, consequently impacting the overall production and homeostatic control of eosinophils [1]. These key biomolecules collectively orchestrate the precise regulation of eosinophil biology.
Pathophysiological Implications of Eosinophil Homeostasis
Section titled “Pathophysiological Implications of Eosinophil Homeostasis”An elevated total eosinophil count, a condition termed eosinophilia, signifies a disruption in the normal hematological balance and can be indicative of various physiological or pathophysiological states. While research has illuminated the genetic underpinnings that contribute to baseline eosinophil levels in healthy populations, these genetic predispositions can also influence an individual’s susceptibility to conditions that lead to further increases[1]. Dysregulation in the homeostatic mechanisms orchestrated by genes such as GATA2, MHC, and HBS1L-MYB can result in either an overproduction or impaired clearance of eosinophils, leading to persistently high counts [1].
Eosinophils, while circulating in the peripheral blood, primarily exert their biological functions within tissues, especially at sites of allergic inflammation or parasitic infection. Consequently, variations observed in peripheral blood eosinophil counts are a systemic reflection of alterations in their production, maturation, or trafficking throughout the body. A comprehensive understanding of the genetic factors influencing baseline eosinophil levels is therefore crucial for distinguishing normal physiological variability from pathological conditions and for advancing research into the genetic basis of eosinophil-associated diseases.
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Elevated total eosinophil count is influenced by a complex interplay of genetic, immunological, and developmental pathways that regulate the production, survival, and mobilization of these immune cells. Genetic studies have identified several loci associated with eosinophil counts, providing insights into the molecular mechanisms underlying their regulation. These pathways encompass critical aspects of cell signaling, gene regulation, and systems-level integration within the hematopoietic and immune systems.
Genetic Determinants of Eosinophil Homeostasis
Section titled “Genetic Determinants of Eosinophil Homeostasis”Genetic variations play a significant role in establishing baseline eosinophil counts, with specific loci identified as modulators of this phenotype. Research indicates that genetic loci within the GATA2, MHC region, and HBS1L-MYB genes are associated with eosinophil counts, suggesting that inherited factors influence the number of these white blood cells[1]. These genetic associations highlight the importance of specific genomic regions in controlling the production and maintenance of eosinophils within the peripheral blood. Variations in these loci can lead to altered gene expression or protein function, thereby influencing the overall pool of circulating eosinophils.
Transcriptional Control of Eosinophil Development
Section titled “Transcriptional Control of Eosinophil Development”The precise regulation of gene expression is fundamental to the differentiation and maturation of eosinophils from hematopoietic stem cells. The GATA2 locus, associated with eosinophil counts, encodes a crucial transcription factor involved in the development of various hematopoietic lineages, including eosinophils[1]. Genetic variations in GATA2 can therefore impact the transcriptional programs that dictate eosinophil commitment, proliferation, and differentiation. Similarly, the HBS1L-MYB locus, also linked to eosinophil counts, contains genes that are known to regulate erythroid and myeloid cell development, implying a role in the broader control of hematopoietic cell fate and maturation pathways[1].
Immune System Modulation and Eosinophil Responses
Section titled “Immune System Modulation and Eosinophil Responses”The Major Histocompatibility Complex (MHC) region is another key genetic locus associated with eosinophil counts, underscoring the interconnectedness of eosinophil regulation with broader immune system functions[1]. The MHC plays a central role in immune recognition and antigen presentation, influencing the activation and recruitment of various immune cells, including eosinophils. Genetic variations within this region can affect the expression of immune-related genes and the signaling pathways that orchestrate inflammatory responses, thereby modulating the survival, activation, and tissue localization of eosinophils. This suggests that the immune environment, shaped by MHC genetics, significantly contributes to the overall eosinophil burden.
Integrated Hematopoietic Regulation and Dysregulation
Section titled “Integrated Hematopoietic Regulation and Dysregulation”The pathways governing eosinophil counts are intricately integrated with other hematopoietic and immune regulatory networks, demonstrating systems-level control. Genetic loci like GATA2, MHC, and HBS1L-MYB influence eosinophil numbers not in isolation, but through crosstalk with other regulatory elements that control diverse aspects of blood cell formation and immune function[1]. Dysregulation within these interconnected pathways, often stemming from genetic variants, can lead to abnormal eosinophil counts, which are relevant to various clinical conditions. Understanding these integrated mechanisms is crucial for identifying potential therapeutic targets that can normalize eosinophil levels by modulating specific components of these complex regulatory networks.
Clinical Relevance
Section titled “Clinical Relevance”Understanding the factors influencing total eosinophil count is crucial for patient care, as variations, including increases, can signify underlying physiological processes or disease states. Recent research, primarily through genome-wide association studies (GWAS), has illuminated the complex genetic architecture that contributes to an individual’s eosinophil levels. These genetic insights provide a foundational understanding that can inform future clinical applications related to eosinophil count variability.
Genetic Predisposition and Risk Stratification
Section titled “Genetic Predisposition and Risk Stratification”Genetic studies have identified multiple loci significantly associated with white blood cell phenotypes, including total eosinophil count[2]. Specifically, analyses have revealed associations between eosinophil counts and genetic variants in regions such as GATA2, the Major Histocompatibility Complex (MHC), and HBS1L-MYB[1]. These genetic insights provide a foundation for understanding individual variability in eosinophil levels, potentially aiding in future risk stratification by identifying individuals genetically predisposed to higher baseline counts or altered immune responses. Such knowledge could eventually inform personalized medicine approaches, though specific applications for managing an increased total eosinophil count based solely on these genetic markers are still under investigation.
Eosinophil Count as a Clinical Indicator
Section titled “Eosinophil Count as a Clinical Indicator”The total white blood cell count, of which eosinophils are a component, is a widely used clinical measure obtained from complete blood count assays [2]. This routine assessment provides a broad overview of an individual’s immune status and can vary considerably across the population [2]. The identification of genetic determinants influencing eosinophil levels suggests that eosinophil count, including an increased total eosinophil count, serves as an observable biomarker. Future research building upon these genetic discoveries may enhance its utility in monitoring disease progression or treatment response, although the current research does not detail such specific clinical applications.
Associations with Broader Hematological Phenotypes
Section titled “Associations with Broader Hematological Phenotypes”The genetic factors influencing eosinophil count often interact within a broader network that shapes various hematological phenotypes[1]. For instance, some genetic loci identified for eosinophil counts may also influence other white blood cell subtypes, highlighting shared or distinct regulatory pathways in hematopoiesis[1]. While these studies primarily focus on identifying genetic associations, understanding these overlapping genetic influences could lead to a more comprehensive view of immune cell dysregulation. This broader perspective may eventually contribute to identifying comorbidities or understanding complex syndromic presentations where an increased total eosinophil count is part of a larger hematological picture.
Frequently Asked Questions About Increased Total Eosinophil Count
Section titled “Frequently Asked Questions About Increased Total Eosinophil Count”These questions address the most important and specific aspects of increased total eosinophil count based on current genetic research.
1. My family has lots of allergies. Will I have high eosinophils too?
Section titled “1. My family has lots of allergies. Will I have high eosinophils too?”Yes, a family history of allergies suggests you might have a genetic predisposition to higher eosinophil counts. Research shows specific genetic regions, like the MHC region, are linked to eosinophil levels and immune responses, which can influence your susceptibility to allergic conditions. While genetics play a role, environmental factors like allergen exposure also contribute significantly.
2. Why is it so hard to know what causes my high eosinophils?
Section titled “2. Why is it so hard to know what causes my high eosinophils?”It’s challenging because many factors influence eosinophil counts, not just a few genes. While some common genetic variants have been identified, much of the total genetic influence comes from rare variants, complex interactions between multiple genes, and the significant interplay with your environment, which are harder to pinpoint. This complexity means that even with advanced studies, a complete picture is still emerging.
3. Can my high eosinophils explain my severe allergies and asthma?
Section titled “3. Can my high eosinophils explain my severe allergies and asthma?”Yes, it can. An increased eosinophil count is often found in people with allergic diseases like asthma and eczema, and these cells contribute to the inflammation that makes symptoms severe and chronic. Monitoring your eosinophil levels helps doctors understand your disease activity and guide treatments that might specifically reduce these cells to improve your condition.
4. Does my ethnic background affect my eosinophil risk?
Section titled “4. Does my ethnic background affect my eosinophil risk?”Yes, your ancestral background can play a role. Genetic studies often focus on specific populations, and findings may not always generalize to others, meaning there might be unique genetic variants or different effect sizes influencing eosinophil counts in your specific ethnic group. This highlights the need for diverse research to understand everyone’s risk better.
5. Can I lower high eosinophils just by avoiding allergens?
Section titled “5. Can I lower high eosinophils just by avoiding allergens?”Avoiding allergens is a good step to manage allergic responses, which can help reduce eosinophil activation. However, genetics also influence your baseline eosinophil count and how your body reacts to allergens. So, while environmental control is important, specific genetic predispositions mean you might still need medical management to effectively lower and control your eosinophil levels.
6. Why do some friends have allergies but normal blood tests?
Section titled “6. Why do some friends have allergies but normal blood tests?”Eosinophil counts are influenced by a complex mix of genetic and environmental factors. While some genetic variants are consistently linked to eosinophil levels, not everyone with allergies will have a clinically high count, and the severity of allergies doesn’t always directly correlate with a single blood test result. Other immune cells and pathways are also involved in allergic reactions, and some genetic influences might be subtle or specific to certain types of allergies.
7. Do antibiotics or other medicines affect my eosinophil test results?
Section titled “7. Do antibiotics or other medicines affect my eosinophil test results?”Yes, certain medications, including antibiotics and steroids, can influence your eosinophil count at the time of a blood test. This is a known confounding factor in clinical assessment. It’s important to inform your doctor about all medications you’re taking, as they can temporarily alter your immune cell levels and potentially affect the interpretation of your results.
8. Can I have high eosinophils without feeling sick or having allergies?
Section titled “8. Can I have high eosinophils without feeling sick or having allergies?”Yes, it is possible. While allergic diseases and parasitic infections are common causes, increased eosinophil counts can sometimes be linked to other less common conditions, such as certain autoimmune disorders or even some types of cancers, even if you don’t have obvious symptoms of these. Your doctor would investigate further to determine the underlying cause if your count is elevated without clear allergic or infectious triggers.
9. Why bother with genetic research if doctors already know about allergies?
Section titled “9. Why bother with genetic research if doctors already know about allergies?”Genetic research helps us understand the fundamental mechanisms behind immune regulation and predispositions to conditions like allergies and asthma, even beyond what we know about environmental triggers. By identifying specific genetic variants influencing eosinophil counts, researchers can develop a deeper understanding of these diseases and potentially lead to new, more targeted therapies that go beyond current treatments for your condition.
10. Do my diet or daily habits influence my eosinophil count?
Section titled “10. Do my diet or daily habits influence my eosinophil count?”Eosinophil counts are highly sensitive to various physiological and environmental factors, which can include allergic exposures from diet and other environmental influences. While genetics set a baseline, your daily habits and environment, including what you eat and your exposure to allergens, can definitely interact with your genetic predispositions to influence how your eosinophil levels fluctuate.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Okada, Y. “Identification of nine novel loci associated with white blood cell subtypes in a Japanese population.” PLoS Genet, 2011.
[2] Nalls, M. A. et al. “Multiple loci are associated with white blood cell phenotypes.” PLoS Genetics, vol. 7, no. 6, 2011, e1002113.
[3] Gudbjartsson, Daniel F., et al. “Sequence Variants Affecting Eosinophil Numbers Associate with Asthma and Myocardial Infarction.”Nature Genetics, vol. 41, no. 3, 2009, pp. 342–347.
[4] Comuzzie, Anthony G. et al. “Novel genetic loci identified for the pathophysiology of childhood obesity in the Hispanic population.”PLoS One, vol. 7, no. 12, 2012, e51954.
[5] Cusanovich, Daniel A., et al. “The combination of a genome-wide association study of lymphocyte count and analysis of gene expression data reveals novel asthma candidate genes.”Human Molecular Genetics, vol. 21, no. 8, 2012, pp. 1656-64.
[6] Crosslin, David R. et al. “Genetic variants associated with the white blood cell count in 13,923 subjects in the eMERGE Network.” Human Genetics, 2011.