Does mating negatively affect female immune defences in insects?

Abstract Immunity is an important mechanism of protection against pathogens and parasites. One factor that can influence immunity is mating. During mating, male-derived materials are transferred to females, and the physical contact also involves the potential risk of sexually transmitted infections, and wounding. Thus, mating can challenge a female’s immune system. This review focuses on exploring how immunity and mating interact in female insects. Although mating has been shown to cause female immune responses in several species, the responses do not always match the observed resistance to pathogens/parasites. Mating up-regulates female immune responses while female resistance is reduced compared to virgin females in some species, and vice versa in other taxa. We discuss why mismatches occur and why post-mating female resistance differs among species, and suggest that measured immune responses may not correlate with female resistance. Also, the mating system will play a major role. Polyandrous mating systems can generate intense post-mating sexual conflict, which can impose high costs of mating on females. Reduced female post-mating resistance may be due to direct suppression of female immunity by males. Alternatively, polyandry may increase the risk of sexually transmitted infections. If this is the major factor driving female post-mating resistance, females of polyandrous species should have higher post-mating immunity. To date, there are insufficient numbers of studies to fully answer the question ‘does mating negatively affect female immune defences in insects?’ To elucidate the links between immunity and mating in females, we need more studies in more species with varied mating systems.

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Microbiome, sex hormones, and immune responses in the reproductive tract: Challenges for vaccine development against sexually transmitted infections

Vaccine ◽

10.1016/j.vaccine.2013.10.010 ◽

2014 ◽

Vol 32 (14) ◽

pp. 1543-1552 ◽

Cited By ~ 46

Author(s):

Rebecca M. Brotman ◽

Jacques Ravel ◽

Patrik M. Bavoil ◽

Patti E. Gravitt ◽

Khalil G. Ghanem

Keyword(s):

Immune Responses ◽

Sexually Transmitted Infections ◽

Sex Hormones ◽

Reproductive Tract ◽

Vaccine Development ◽

Sexually Transmitted

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The Impact of MTHFR 1298 A > C and 677 C > T Gene Polymorphisms as Susceptibility Risk Factors in Cervical Intraepithelial Neoplasia Related to HPV and Sexually Transmitted Infections

The Journal of Obstetrics and Gynecology of India ◽

10.1007/s13224-020-01363-z ◽

2020 ◽

Vol 70 (6) ◽

pp. 503-509

Author(s):

Amir Sohrabi ◽

Fatemeh Bassam-Tolami ◽

Mohsen Imani

Keyword(s):

Risk Factors ◽

Cervical Intraepithelial Neoplasia ◽

Sexually Transmitted Infections ◽

Cancer Progression ◽

Potential Risk ◽

Intraepithelial Neoplasia ◽

Sexually Transmitted ◽

Significant Difference ◽

Hpv Genotypes ◽

The Impact

Abstract Background HPV genotypes are the most common etiological factor for genital neoplasia. It would appear that sexually transmitted infections accompanied with HPV genotypes might have synergistic interactions in cancer progression. The genetic polymorphisms are involved in metabolizing carcinogens which may contribute to the susceptibility of developing genital cancers by less efficient or overly down metabolic pathways and cell signaling. MTHFR polymorphisms are related to several metabolic disorders and human cancers. We investigated the contribution of MTHFR 1298 and MTHFR 677 polymorphisms as potential risk factors for outcomes with HPV genotypes and STIs in Iranian population. Materials and Methods As a case–control study, MTHFR A1298C and C677T were assessed for SNPs analysis using a PCR–RFLP assay in 50 cervical intraepithelial neoplasia (CIN) cases, 98 HPV-positive subjects and 47 non-cancerous/non-HPV patients as healthy controls. Results Finding suggested a significant association between the MTHFR 1298 CC polymorphisms (OR = 3.5, 95% CI = 1.13–10.82, P ≤ 0.05) in women with CIN as compared to non-cancerous/non-HPV subjects. There was not a significant difference of MTHFR 677 between outcomes. Discussion It would seem MTHFR 1298 CC is more likely to be a potential risk factor for HPV–cervical cancer progression. Consequences support further attempts to understand the clinical manifestations of neoplasia related to genital infections and gene mutations.

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Convergent Evolution by Cancer and Viruses in Evading the NKG2D Immune Response

Cancers ◽

10.3390/cancers12123827 ◽

2020 ◽

Vol 12 (12) ◽

pp. 3827

Author(s):

Richard Baugh ◽

Hena Khalique ◽

Leonard W. Seymour

Keyword(s):

Immune System ◽

Immune Responses ◽

Cancer Cells ◽

Innate Immune System ◽

Cell Transformation ◽

Innate Immune ◽

Immune Mediated ◽

Pathogenic Viruses ◽

Group 2 ◽

Immune Defences

The natural killer group 2 member D (NKG2D) receptor and its family of NKG2D ligands (NKG2DLs) are key components in the innate immune system, triggering NK, γδ and CD8+ T cell-mediated immune responses. While surface NKG2DL are rarely found on healthy cells, expression is significantly increased in response to various types of cellular stress, viral infection, and tumour cell transformation. In order to evade immune-mediated cytotoxicity, both pathogenic viruses and cancer cells have evolved various mechanisms of subverting immune defences and preventing NKG2DL expression. Comparisons of the mechanisms employed following virus infection or malignant transformation reveal a pattern of converging evolution at many of the key regulatory steps involved in NKG2DL expression and subsequent immune responses. Exploring ways to target these shared steps in virus- and cancer-mediated immune evasion may provide new mechanistic insights and therapeutic opportunities, for example, using oncolytic virotherapy to re-engage the innate immune system towards cancer cells.

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Sexually transmitted infections in polygamous mating systems

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2012.0048 ◽

2013 ◽

Vol 368 (1613) ◽

pp. 20120048 ◽

Cited By ~ 38

Author(s):

Ben Ashby ◽

Sunetra Gupta

Keyword(s):

Sexually Transmitted Infections ◽

Mating Systems ◽

Disease Incidence ◽

Sexual Contact ◽

Small Subset ◽

Sexually Transmitted ◽

Pathogen Virulence ◽

Contact Patterns ◽

Transmission Pathways ◽

The Impact

Sexually transmitted infections (STIs) are often associated with chronic diseases and can have severe impacts on host reproductive success. For airborne or socially transmitted pathogens, patterns of contact by which the infection spreads tend to be dispersed and each contact may be of very short duration. By contrast, the transmission pathways for STIs are usually characterized by repeated contacts with a small subset of the population. Here we review how heterogeneity in sexual contact patterns can influence epidemiological dynamics, and present a simple model of polygyny/polyandry to illustrate the impact of biased mating systems on disease incidence and pathogen virulence.

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Chlamydia trachomatisLipopolysaccharide Evades the Canonical and Noncanonical Inflammatory Pathways To Subvert Innate Immunity

mBio ◽

10.1128/mbio.00595-19 ◽

2019 ◽

Vol 10 (2) ◽

Cited By ~ 7

Author(s):

Chunfu Yang ◽

Michael Briones ◽

Janice Chiou ◽

Lei Lei ◽

Michael John Patton ◽

...

Keyword(s):

Innate Immunity ◽

Chlamydia Trachomatis ◽

Immune Responses ◽

Sexually Transmitted Infections ◽

Outer Membrane ◽

Content Type ◽

Sexually Transmitted ◽

Inflammatory Pathways ◽

High Incidence ◽

Potent Agonist

ABSTRACTChlamydia trachomatisis the most common bacterial cause of sexually transmitted infections.C. trachomatissexually transmitted infections are commonly asymptomatic, implying a pathogenic strategy for the evasion of innate inflammatory immune responses, a paradox as theC. trachomatisouter membrane contains lipopolysaccharide (LPS), a known potent agonist of inflammatory innate immunity. Here, we studied the ability of chlamydial LPS to activate the proinflammatory canonical and noncanonical inflammasome pathways in mouse bone marrow-derived macrophages (BMDM). We show, in comparison toEscherichiacoliLPS, thatC. trachomatisLPS-treated BMDM produce significantly less IL-6, TNF, and type I interferon mRNA, indicating that downstream signaling through the canonical TLR4 myddosome and triffosome pathways was blocked. We confirmed this inC. trachomatisLPS-treated BMDM by showing the lack of NF-κB and IRF3 phosphorylation, respectively. Interestingly,C. trachomatisLPS bound CD14 and promoted its endocytosis; however; it did not promote efficient TLR4/MD-2 dimerization or endocytosis, known requirements for myddosome and triffosome signaling pathways. We further found that transfection of BMDM withC. trachomatisLPS did not cause pyroptotic cell ballooning, cytotoxicity, or IL-1β secretion, all characteristic features of noncanonical inflammasome activation. Western blotting confirmed that cytosolicC. trachomatisLPS failed to signal through caspase-11, as shown by the lack of gasdermin D, caspase-1, or IL-1β proteolytic cleavage. We propose that chlamydiae evolved a unique LPS structure as a pathogenic strategy to avoid canonical and noncanonical innate immune signaling and conclude that this strategy might explain the high incidence of asymptomatic infections.IMPORTANCEChlamydia trachomatisis the most common bacterial cause of sexually transmitted infections (STI).C. trachomatisSTI are commonly asymptomatic, implying a pathogenic strategy for the evasion of innate inflammatory immune responses, a paradox as theC. trachomatisouter membrane contains lipopolysaccharide (LPS), a known potent agonist of inflammatory innate immunity. Here, we found thatC. trachomatisLPS is not capable of engaging the canonical TLR4/MD-2 or noncanonical caspase-11 inflammatory pathways. The inability ofC. trachomatisLPS to trigger innate immunity inflammatory pathways is related to its unique fatty acid structure. Evolutionary modification of the LPS structure likely evolved as a pathogenic strategy to silence innate host defense mechanisms. The findings might explain the high incidence of asymptomatic chlamydial genital infection.

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