Sex differences shape the response to infectious diseases

Ingersoll, Molly A.

doi:10.1371/journal.ppat.1006688

Cited by 93 publications

(79 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In fact, the prevalence of anti-WNV antibodies is similar in females and males in endemic areas and the increased exposure due to outdoor activities is not sufficient to explain sex differences in the incidence of WNND [25]. Although experimental studies on the role of gender in the development of WNV encephalitis are lacking, sex differences in innate and adaptive immune responses might account for the higher prevalence and severity of WNV disease in males [26,27]. Intriguingly, in this study, the incidence rate of WNV infection was also higher in male than in female blood donors, suggesting a gender-biased risk of infection.…”

Section: Discussionmentioning

confidence: 99%

Human West Nile Virus Lineage 2 Infection: Epidemiological, Clinical, and Virological Findings

Pacenti

Sinigaglia

Franchin

et al. 2020

Viruses

View full text Add to dashboard Cite

West Nile virus (WNV) lineage 2 is expanding and causing large outbreaks in Europe. In this study, we analyzed the epidemiological, clinical, and virological features of WNV lineage 2 infection during the large outbreak that occurred in northern Italy in 2018. The study population included 86 patients with neuroinvasive disease (WNND), 307 with fever (WNF), and 34 blood donors. Phylogenetic analysis of WNV full genome sequences from patients’ samples showed that the virus belonged to the widespread central/southern European clade of WNV lineage 2 and was circulating in the area at least since 2014. The incidence of WNND and WNF progressively increased with age and was higher in males than in females. Among WNND patients, the case fatality rate was 22%. About 70% of blood donors reported symptoms during follow-up. Within the first week after symptom onset, WNV RNA was detectable in the blood or urine of 80% of patients, while 20% and 40% of WNND and WNF patients, respectively, were WNV IgM-seronegative. In CSF samples of WNND patients, WNV RNA was typically detectable when WNV IgM antibodies were absent. Blunted or no WNV IgM response and high WNV IgG levels were observed in seven patients with previous flavivirus immunity.

show abstract

Section: Discussionmentioning

confidence: 99%

Human West Nile Virus Lineage 2 Infection: Epidemiological, Clinical, and Virological Findings

Pacenti

Sinigaglia

Franchin

et al. 2020

Viruses

View full text Add to dashboard Cite

show abstract

“…Thus, future IVM studies, perhaps using multiple chronic windows, to visualize immune responses over the course of ascending UTI would be very interesting. Moreover, a clear sex bias in the risk and prevalence of UTIs exists, with women being much more susceptible than men . Although this disparity is largely ascribed to anatomic differences, mounting evidence suggests that estrogen and other sex‐specific molecules broadly influence the host immune response .…”

Section: Localized Infectionsmentioning

confidence: 99%

Unraveling the host's immune response to infection: Seeing is believing

Scott

Sarkar

Kratofil

et al. 2019

Journal of Leukocyte Biology

View full text Add to dashboard Cite

It has long been appreciated that understanding the interactions between the host and the pathogens that make us sick is critical for the prevention and treatment of disease. As antibiotics become increasingly ineffective, targeting the host and specific bacterial evasion mechanisms are becoming novel therapeutic approaches. The technology used to understand host‐pathogen interactions has dramatically advanced over the last century. We have moved away from using simple in vitro assays focused on single‐cell events to technologies that allow us to observe complex multicellular interactions in real time in live animals. Specifically, intravital microscopy (IVM) has improved our understanding of infection, from viral to bacterial to parasitic, and how the host immune system responds to these infections. Yet, at the same time it has allowed us to appreciate just how complex these interactions are and that current experimental models still have a number of limitations. In this review, we will discuss the advances in vivo IVM has brought to the study of host‐pathogen interactions, focusing primarily on bacterial infections and innate immunity.

show abstract

“…Allcause prostatitis develops in nearly 10% of all men, with increased risks of chronicity after the age of fifty (Krieger et al, 2008;Schaeffer, 2003). Prostatitis is more common in the elderly, similar to urinary tract infection in men (Foxman, 2010;Ingersoll, 2017;Khan et al, 2017;Lipsky, 1999;Rowe and Juthani-Mehta, 2013). An estimated 10% of all prostatitis cases are due to bacterial infection (Khan et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

The immune system fails to mount a protective response to Gram-positive or Gram-negative bacterial prostatitis

Lupo

Rousseau

Canton

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Bacterial prostatitis affects 1% of men, with increased incidence in the elderly. It is defined by the frequency and urgency to urinate, localized pain, and positive bacterial cultures in expressed seminal fluids. Acute bacterial prostatitis frequently progresses to chronicity, which is marked by recurrent acute episodes interspersed with asymptomatic periods of variable duration. Up to 80% of bacterial prostatitis cases are caused by Gram-negative uropathogenic E. coli (UPEC) or Gram-positive E. faecalis. Antibiotic treatment is standard of care, however, global dissemination of antimicrobial resistant uropathogens threatens efficacy of therapy. Thus, development of non-antibiotic-based approaches to treat bacterial prostatitis is a priority. One challenge is that the immune response to infection in the prostate is incompletely understood. We used a mouse model of transurethral bacterial instillation to study the immune response to UPEC or E. faecalis prostate infection. Both uropathogens exhibited tropism for the prostate over the bladder early post-infection. UPEC infection induced greater proinflammatory cytokine expression and neutrophil and monocyte infiltration compared to E. faecalis infection. Following challenge infection, cytokine responses and myeloid cell infiltration were largely comparable to primary infection.Characteristic of memory responses, more lymphoid cells infiltrating the prostate in the second infection compared to the primary infection. Unexpectedly, however, bacterial burden in prostates challenged with either UPEC or E. faecalis was equal or greater than in primary infection, despite that an adaptive response to UPEC infection was evident in the bladder of the same animals. Thus, an immune response to primary infection is initiated, however it does not protect against reinfection. Our findings support the idea that chronic or recurrent prostatitis develops in the absence of efficacious immunity to infection. A greater understanding of the mechanisms underlying this observation may point to actionable targets for immunotherapy.

show abstract

Sex differences shape the response to infectious diseases

Abstract: International audienceHistorically, we have overlooked sex as a variable in infectious disease research

Cited by 93 publications

References 35 publications

Human West Nile Virus Lineage 2 Infection: Epidemiological, Clinical, and Virological Findings

Human West Nile Virus Lineage 2 Infection: Epidemiological, Clinical, and Virological Findings

Unraveling the host's immune response to infection: Seeing is believing

The immune system fails to mount a protective response to Gram-positive or Gram-negative bacterial prostatitis

Contact Info

Product

Resources

About