Sex differences in melanotic encapsulation responses (immunocompetence) in the damselfly Lestes forcipatus Rambur

2002 ◽  
Vol 80 (9) ◽  
pp. 1578-1583 ◽  
Author(s):  
Christopher P Yourth ◽  
Mark R Forbes ◽  
Robert L Baker

A few studies have shown that male and female invertebrates differ in immunity and that these differences appear related to differences in sexual dimorphism and gender differences in life histories. Melanotic encapsulation of foreign objects in insects is one form of immunity. The damselfly Lestes forcipatus Rambur is moderately sexually dimorphic, and much is known about patterns of mass gain in congeners relating to differences in life history between males and females. In this study, females were more immunoresponsive than males under controlled temperatures, following emergence, and at a time when parasitic mites were challenging these hosts. However, males and females that overlapped in mass at emergence did not differ in their immune responses. Males in better condition at emergence were more immunoresponsive than lighter males, but this relation was not found in females. Sex differences in immune expression may have implications for how females versus males are able to deal with challenges from parasites, under varying environmental conditions.

2018 ◽  
Vol 373 (1757) ◽  
pp. 20170431 ◽  
Author(s):  
Matthew D. Hall ◽  
Nicole Mideo

Sex differences in the prevalence, course and severity of infection are widespread, yet the evolutionary consequences of these differences remain unclear. Understanding how male–female differences affect the trajectory of infectious disease requires connecting the contrasting dynamics that pathogens might experience within each sex to the number of susceptible and infected individuals that are circulating in a population. In this study, we build on theory using genetic covariance functions to link the growth of a pathogen within a host to the evolution and spread of disease between individuals. Using the Daphnia–Pasteuria system as a test case, we show that on the basis of within-host dynamics alone, females seem to be more evolutionarily liable for the pathogen, with higher spore loads and greater divergence among pathogen genotypes as infection progresses. Between-host transmission, however, appears to offset the lower performance of a pathogen within a male host, making even subtle differences between the sexes evolutionarily relevant, as long as the selection generated by the between-host dynamics is sufficiently strong. Our model suggests that relatively simple differences in within-host processes occurring in males and females can lead to complex patterns of genetic constraint on pathogen evolution, particularly during an expanding epidemic. This article is part of the theme issue ‘Linking local adaptation with the evolution of sex differences’.


Author(s):  
Daniel Enrique Rodriguez Bauza ◽  
Patricia Silveyra

Exercise-induced bronchoconstriction (EIB) is a common complication of athletes and individuals who exercise regularly. It is estimated that about 90% of patients with underlying asthma (a sexually dimorphic disease) experience EIB; however, sex differences in EIB have not been studied extensively. With the goal of better understanding the prevalence of EIB in males and females, and because atopy has been reported to occur at higher rates in athletes, in this study, we investigated sex differences in EIB and atopy in athletes. A systematic literature review identified 60 studies evaluating EIB and/or atopy in post-pubertal adult athletes (n = 7501). Collectively, these studies reported: (1) a 23% prevalence of EIB in athletes; (2) a higher prevalence of atopy in male vs. female athletes; (3) a higher prevalence of atopy in athletes with EIB; (4) a significantly higher rate of atopic EIB in male vs. female athletes. Our analysis indicates that the physiological changes that occur during exercise may differentially affect male and female athletes, and suggest an interaction between male sex, exercise, and atopic status in the course of EIB. Understanding these sex differences is important to provide personalized management plans to athletes with underlying asthma and/or atopy.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ajay Pradhan ◽  
Per-Erik Olsson

Abstract Coronavirus disease 2019 (COVID-19) has shown high infection and mortality rates all over the world, and despite the global efforts, there is so far no specific therapy available for COVID-19. Interestingly, while the severity and mortality of COVID-19 are higher in males than in females, the underlying molecular mechanisms are unclear. In this review, we explore sex-related differences that may be contributing factors to the observed male-biased mortality from COVID-19. Males are considered the weaker sex in aspects related to endurance and infection control. Studies show that viral RNA clearance is delayed in males with COVID-19. A recent study has indicated that the testis can harbor coronavirus, and consequently, males show delayed viral clearance. However, the role of testis involvement in COVID-19 severity and mortality needs further research. Males and females show a distinct difference in immune system responses with females eliciting stronger immune responses to pathogens. This difference in immune system responses may be a major contributing factor to viral load, disease severity, and mortality. In addition, differences in sex hormone milieus could also be a determinant of viral infections as estrogen has immunoenhancing effects while testosterone has immunosuppressive effects. The sex-specific severity of COVID-19 infections indicates that further research on understanding the sex differences is needed. Inclusion of both males and females in basic research and clinical trials is required to provide critical information on sex-related differences that may help to better understand disease outcome and therapy.


2019 ◽  
Author(s):  
Pui-Pik Law ◽  
Ping-Kei Chan ◽  
Kirsten McEwen ◽  
Huihan Zhi ◽  
Bing Liang ◽  
...  

SummarySex differences in growth rate in very early embryos have been recognized in a variety of mammals and attributed to sex-chromosome complement effects as they occur before overt sexual differentiation. We previously found that sex-chromosome complement, rather than sex hormones regulates heterochromatin-mediated silencing of a transgene and autosomal gene expression in mice. Here, sex dimorphism in proliferation was investigated. We confirm that male embryonic fibroblasts proliferate faster than female fibroblasts and show that this proliferation advantage is completely dependent upon heterochromatin protein 1 gamma (HP1γ). To determine whether this sex-regulatory effect of HP1γ was a more general phenomenon, we performed RNA sequencing on MEFs derived from males and females, with or without HP1γ. Strikingly, HP1γ was found to be crucial for regulating nearly all sexually dimorphic autosomal gene expression because deletion of the HP1γ gene in males abolished sex differences in autosomal gene expression. The identification of a key epigenetic modifier as central in defining gene expression differences between males and females has important implications for understanding physiological sex differences and sex bias in disease.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Hajar Amini ◽  
Bodie Knepp ◽  
Heather Hull ◽  
Paulina Carmona-Mora ◽  
Marisa Hakoupian ◽  
...  

Objective: Ischemic stroke (IS) is sexually dimorphic for risk factors, age, heritability, causes, treatment, and outcome. We identified transcriptional correlates with 90-day outcome that differed between male and female IS subjects. Methods: RNA from 72 samples from 2 peripheral blood draws (at ≤3 and 24h post IS onset) was analyzed on Affymetrix U133 Plus 2 microarrays. These represented samples from 36 CLEAR trial IS patients treated with tPA with or without eptifibatide after the first blood sample within 3 hours of stroke onset. Changes in gene expression levels (deltaGE) between 3h and 24h were calculated and the association with percent NIH Stroke Scale (NIHSS) improvement from 3h to 90 days (% Improvement) examined. We used mixed-effects linear regression, including Treatment, Age, Sex, Vascular Risk Factors, 3h NIHSS, % Improvement, and a Sex * % Improvement interaction. Sex differences in association of gene expression with % Improvement were determined by examining the Sex * % Improvement interaction term, p<0.005 was considered statistically significant. Results: 577 genes correlated differently with % Improvement in IS males and females. These included matrix metalloproteinases (MMPs), which play a major role in BBB dysfunction and outcomes post IS. MMP11 , MMP14 and MM17 correlated with % Improvement in opposite direction in males and females. Inflammatory genes like IL-27 , implicated in infarct volume and stroke outcome, and ABC transporters ( ABCC9 ) also had opposite correlation with % Improvement in males and females. Calmodulin 1 ( CAML1 ) was also sexually dimorphic, and a SNP in CALM1 has been implicated in IS risk and blood coagulation in female IS patients. EIF2 signaling, a major protein synthesis pathway was activated in males (adj. p = 1e-8), while suppressed in females (adj. p value = 1e-9). Protein synthesis and associated unfolded protein response cascade have previously been implicated in stroke outcome. Conclusions: The identified sexually dimorphic gene expression associated with 90-day improvement might relate to sex differences in blood immune and clotting pathways. The findings expand our understanding of the genomic underpinnings associated with stroke outcome and may serve as potential sex-specific treatment targets.


Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1875-1886 ◽  
Author(s):  
Sheila J. Semaan ◽  
Sangeeta Dhamija ◽  
Joshua Kim ◽  
Eric C. Ku ◽  
Alexander S. Kauffman

The Kiss1 gene, which encodes kisspeptin and is critical for reproduction, is sexually differentiated in the hypothalamic anteroventral periventricular (AVPV)/rostral periventricular (PeN) nuclei. Specifically, female rodents have higher AVPV/PeN Kiss1 expression than males, but how this Kiss1 sex difference is induced in early development is poorly understood. Here, we explored the contribution of epigenetic mechanisms to the establishment of the AVPV/PeN Kiss1 sex difference, focusing on histone deacetylation and DNA methylation. First, we utilized postnatal pharmacological blockade of histone deacetylation and analyzed Kiss1 expression in the AVPV/PeN. Postnatal disruption of histone deacetylase modestly increased AVPV Kiss1 cell number in both sexes but did not alter the Kiss1 sex difference. Next, we assessed whether the level of CpG methylation, which can influence transcription factor binding and gene expression, in the murine Kiss1 gene differs between males and females. We found significant sex differences in methylation at several CpG sites in the putative promoter and first intron of the Kiss1 gene in the AVPV/PeN, but not in the arcuate (which lacks adult Kiss1 sex differences), suggesting that differential methylation of the Kiss1 gene may influence sexually-dimorphic Kiss1 expression in the AVPV/PeN. Transgenic impairment of methyl CpG-binding protein-2 function did not eliminate the Kiss1 sex difference, indicating that other methylation factors are involved. Interestingly, CpG methylation in the AVPV/PeN was lower in males than females, suggesting that transcriptional repressors may contribute to the AVPV/PeN Kiss1 sex difference, a possibility supported by in silico identification of putative repressor binding sites near some of the sexually-dimorphic CpG.


2016 ◽  
Vol 311 (2) ◽  
pp. R211-R216 ◽  
Author(s):  
C. Griffin ◽  
N. Lanzetta ◽  
L. Eter ◽  
K. Singer

It is well known in clinical and animal studies that women and men have different disease risk as well as different disease physiology. Women of reproductive age are protected from metabolic and cardiovascular disease compared with postmenopausal women and men. Most murine studies are skewed toward the use of male mice to study obesity-induced metabolic dysfunction because of similar protection in female mice. We have investigated dietary obesity in a mouse model and have directly compared inflammatory responses in males and females. In this review we will summarize what is known about sex differences in diet-induced inflammation and will summarize our data on this topic. It is clear that sex differences in high-fat diet-induced inflammatory activation are due to cell intrinsic differences in hematopoietic responses to obesogenic cues, but further research is needed to understand what leads to sexually dimorphic responses.


2004 ◽  
Vol 5 (4) ◽  
pp. 243-254 ◽  
Author(s):  
Duck-Hee Kang ◽  
Chun-Ja Kim ◽  
Yeonok Suh

The immune system is the body’s major defense mechanism against disease. However, psychosocial factors, such as stress, can modulate various immune responses. Although they have been examined in adult humans and other animals, sex differences in immune responses and immune reactivity to stress have rarely been examined in adolescents, particularly comparing healthy and asthmatic adolescents. In 151 healthy and asthmatic high school adolescents (91 females and 60 males), natural killer cell (NK) cytotoxicity, polymorphonuclear leukocyte (PMN) superoxide release, lymphocyte proliferative responses, and CD subsets were measured twice: once during mid-semester and again during final examinations. There was little difference in these measures between healthy and asthmatic adolescents. Similarly, only sex difference was noted in NK cytotoxicity at a 25:1 effector-to-target cell ratio, with males showing significantly higher responses than females. For PMN superoxide release, females significantly increased their responses during final examinations, whereas males demonstrated no changes. For lymphocyte proliferative responses, both females and males increased their responses during final examinations, but the magnitude of increase was much greater in males. Furthermore, racial comparisons indicated that African American adolescents (n = 16), as compared with Caucasian adolescents (n = 128), had significantly higher responses in PMN superoxide release to N-Formyl-Met-Leu-Phe (FMLP) activation during mid-semester and lymphocyte proliferative responses at both time points. Nevertheless, the overall findings indicate limited differences in immune responses and immune reactivity to stress in adolescents between males and females, healthy and asthmatic adolescents, and Caucasians and African Americans. However, further investigations with larger samples are warranted.


2008 ◽  
Vol 86 (7) ◽  
pp. 610-622 ◽  
Author(s):  
Rosana Paredes ◽  
Ian L. Jones ◽  
Daryl J. Boness ◽  
Yann Tremblay ◽  
Martin Renner

At the Gannet Islands, Labrador, sympatric thick-billed murres ( Uria lomvia (L., 1758)) and razorbills ( Alca torda L., 1758) are slightly sexually dimorphic and have similar intersexual differences in parental roles; females are the main meal providers and males are mostly involved in brooding and chick defence at the breeding site and at sea. The question is whether differences in parental roles influence the foraging behaviour patterns of males and females. Murre females foraged during twilight periods and dived shallower than males. In razorbills, although sex differences were not as clear, females also tended to dive shallower (<10 m) and more often at twilight. Males of both species foraged during daylight hours and tended to dive deeper than females. Females of both species had shorter dive bouts (i.e., duration of a series of dives) even though the number of bouts and dives per day were equal between sexes. In both species, female dives were mostly shallower W-shaped dives, likely for capturing crustaceans at twilight. In contrast, males performed mostly deeper U-shaped dives for capturing mid-water species (e.g., capelin, Mallotus villosus (Müller, 1776)). Altogether, our results show that the two sympatric auks had relatively similar intersexual segregation in feeding time, depth, and prey. Sex differences in nest attendance, driven by differences in parental roles, seem to explain these findings.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e16051-e16051
Author(s):  
Elizabeth Pan ◽  
Ugonna Ihenacho ◽  
Victoria Cortesssis ◽  
Syem Barakzai ◽  
James S Hu

e16051 Background: Germ cell tumors (GCT) commonly arise in post pubertal gonads where they are influenced by sexually dimorphic hormone signaling. More rarely, extra-gonadal GCTs (EGGCTs) arise in midline sites, coinciding with the route of primordial germ cell migration. EGGCTs are proposed to arise from cells not completing this migration. We characterized the incidence of EGGCTs according to patient and tumor features in an attempt to elucidate tumor origins. Methods: In Surveillance, Epidemiology, and End Results (SEER) Program SEER*Stat Database SEER 9 Regs Research Data, 1973-2015, primary EGGCT cases were identified by ICD-O-3 histologic types (seminoma: 9060-9062, 9064; non-seminoma 9065-9101) grouped into central nervous system (CNS), mediastinum, and other EGGCT sites. Age-specific incidences for males and females were divided into adolescents and young adults (AYA) defined by the National Cancer Institute as 15-39 years of age, and younger childhood and older adult groups. Results: In AYAs and older adults, age-adjusted incidence of males exceeded that of females at all sites (p≤0.006, all comparisons) (Table). Male incidence was highest in AYAs (all EGGCT, 4.35/1,000,000 person-years (Mpy); mediastinum, 2.17/Mpy; other 0.68/Mpy). Female incidence was highest in childhood (CNS, 0.86/Mpy; mediastinum, 0.14/Mpy; other 0.64/Mp-y). Conclusions: Patterns of EGGCT incidence differ substantially between sexes. Permissive extra-gonadal sites of males or male-predominant exposures may explain higher incidence in males. Alternatively, EGGCT precursor cells may have sex-specific features affecting malignant potential. [Table: see text]


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