Oxford open immunologyPub Date : 2024-08-17eCollection Date: 2024-01-01DOI: 10.1093/oxfimm/iqae010
Kar On Cheng, Dolly E Montaño, Teresa Zelante, Axel Dietschmann, Mark S Gresnigt
{"title":"Inflammatory cytokine signalling in vulvovaginal candidiasis: a hot mess driving immunopathology.","authors":"Kar On Cheng, Dolly E Montaño, Teresa Zelante, Axel Dietschmann, Mark S Gresnigt","doi":"10.1093/oxfimm/iqae010","DOIUrl":"10.1093/oxfimm/iqae010","url":null,"abstract":"<p><p>Protective immunity to opportunistic fungal infections consists of tightly regulated innate and adaptive immune responses that clear the infection. Immune responses to infections of the vaginal mucosa by <i>Candida</i> species are, however, an exception. In the case of vulvovaginal candidiasis (VVC), the inflammatory response is associated with symptomatic disease, rather than that it results in pathogen clearance. As such VVC can be considered an inflammatory disease, which is a significant public health problem due to its predominance as a female-specific fungal infection. Particularly, women with recurrent VVC (RVVC) suffer from a significant negative impact on their quality of life and mental health. Knowledge of the inflammatory pathogenesis of (R)VVC may guide more effective diagnostic and therapeutic options to improve the quality of life of women with (R)VVC. Here, we review the immunopathogenesis of (R)VVC describing several elements that induce an inflammatory arson, starting with the activation threshold established by vaginal epithelial cells that prevent unnecessary ignition of inflammatory responses, epithelial and inflammasome-dependent immune responses. These inflammatory responses will drive neutrophil recruitment and dysfunctional neutrophil-mediated inflammation. We also review the, sometimes controversial, findings on the involvement of adaptive and systemic responses. Finally, we provide future perspectives on the potential of some unexplored cytokine axes and discuss whether VVC needs to be subdivided into subgroups to improve diagnosis and treatment.</p>","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"5 1","pages":"iqae010"},"PeriodicalIF":0.0,"publicationDate":"2024-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142135096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxford open immunologyPub Date : 2024-07-26eCollection Date: 2024-01-01DOI: 10.1093/oxfimm/iqae007
{"title":"Correction to: <i>In-vitro</i> assessment of cutaneous immune responses to <i>aedes</i> mosquito salivary gland extract and dengue virus in Cambodian individuals.","authors":"","doi":"10.1093/oxfimm/iqae007","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae007","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/oxfimm/iqae003.].</p>","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"5 1","pages":"iqae007"},"PeriodicalIF":0.0,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11281826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The gut-lung axis: the impact of the gut mycobiome on pulmonary diseases and infections","authors":"Emily Sey, A. Warris","doi":"10.1093/oxfimm/iqae008","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae008","url":null,"abstract":"\u0000 The gastrointestinal tract contains a diverse microbiome consisting of bacteria, fungi, viruses and archaea. Although these microbes usually reside as commensal organisms, it is now well established that higher abundance of specific bacterial or fungal species, or loss of diversity in the microbiome can significantly affect development, progression and outcomes in disease. Studies have mainly focused on the effects of bacteria, however, the impact of other microbes, such as fungi, has received increased attention in the last few years. Fungi only represent around 0.1% of the total gut microbial population. However, key fungal taxa such as Candida, Aspergillus and Wallemia have been shown to significantly impact health and disease. The composition of the gut mycobiome has been shown to affect immunity at distal sites, such as the heart, lung, brain, pancreas, and liver. In the case of the lung this phenomenon is referred to as the “gut-lung axis”. Recent studies have begun to explore and unveil the relationship between gut fungi and lung immunity in diseases such as asthma and lung cancer, and lung infections caused by viruses, bacteria and fungi. In this review we will summarise the current, rapidly growing, literature describing the impact of the gut mycobiome on respiratory disease and infection.","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"12 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141808594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxford open immunologyPub Date : 2024-06-14eCollection Date: 2024-01-01DOI: 10.1093/oxfimm/iqae006
Norifumi Iijima
{"title":"The emerging role of effector functions exerted by tissue-resident memory T cells.","authors":"Norifumi Iijima","doi":"10.1093/oxfimm/iqae006","DOIUrl":"10.1093/oxfimm/iqae006","url":null,"abstract":"<p><p>The magnitude of the effector functions of memory T cells determines the consequences of the protection against invading pathogens and tumor development or the pathogenesis of autoimmune and allergic diseases. Tissue-resident memory T cells (T<sub>RM</sub> cells) are unique T-cell populations that persist in tissues for long periods awaiting re-encounter with their cognate antigen. Although T<sub>RM</sub> cell reactivation primarily requires the presentation of cognate antigens, recent evidence has shown that, in addition to the conventional concept, T<sub>RM</sub> cells can be reactivated without the presentation of cognate antigens. Non-cognate T<sub>RM</sub> cell activation is triggered by cross-reactive antigens or by several combinations of cytokines, including interleukin (IL)-2, IL-7, IL-12, IL-15 and IL-18. The activation mode of T<sub>RM</sub> cells reinforces their cytotoxic activity and promotes the secretion of effector cytokines (such as interferon-gamma and tumor necrosis factor-alpha). This review highlights the key features of T<sub>RM</sub> cell maintenance and reactivation and discusses the importance of effector functions that T<sub>RM</sub> cells exert upon being presented with cognate and/or non-cognate antigens, as well as cytokines secreted by T<sub>RM</sub> and non-T<sub>RM</sub> cells within the tissue microenvironment.</p>","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"5 1","pages":"iqae006"},"PeriodicalIF":0.0,"publicationDate":"2024-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11213632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142082871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vasile Mihai Sularea, Ruchi Sharma, David C Hay, Cliona O’Farrelly
{"title":"Early interferon lambda production is induced by double-stranded RNA in iPS-derived hepatocyte-like cells","authors":"Vasile Mihai Sularea, Ruchi Sharma, David C Hay, Cliona O’Farrelly","doi":"10.1093/oxfimm/iqae004","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae004","url":null,"abstract":"\u0000 Hepatotropic viruses are amongst the most ubiquitous pathogens worldwide, causing significant morbidity and mortality. As hepatocytes are among the primary targets of these viruses, their ability to mount early effective innate defence responses is of major research interest. Interferon lambda (IFNL) is produced early in response to viral stimulation in other cell types, but hepatocyte production of this interferon is little investigated. Due to the difficulty and significant costs in obtaining and culturing human primary hepatocytes, surrogate systems are widely sought. Here we used induced pluripotent stem (iPS)-derived hepatocyte-like cells (HLCs) to investigate hepatic IFNL expression in response to viral-like ligands. We demonstrate that hepatocytes rely on cytoplasmic pattern recognition receptors (PRRs) such as Protein Kinase RNA-dependent (PKR) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLR) for the detection of double stranded RNA. Stimulation of HLCs by viral-like RNA ligands activating cytosolic RNA sensors resulted in thousand fold increase of type III interferon gene expression. These results are in contrast with type I IFN expression, which was induced to a lower extent. Concomitant induction of interferon stimulated genes, such as interferon-stimulated gene 15 (ISG15) and CXCL10, indicated the ability of HLCs to activate interferon-dependent activity. These results demonstrate that HLCs mount an innate antiviral response upon stimulation with viral-like RNA characterised by the induction of type III IFN.","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"204 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141376075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chanh Ho Quang, Trieu Huynh Trung, Tam Dong Thi Hoai, Tran Kim Hung, Huynh Ngoc Thien Vuong, Phan Tu Qui, Huyen Vu Ngo Thanh, Alexandra Moncada, Thanh Kieu Nguyen Thi, Duyen Huynh Thi Le, Ngan Nguyen-Lyle, Vuong Nguyen Lam, Lam Phung Khanh, Angela McBride, Bridget Wills, Sophie Yacoub
{"title":"Kinetics of cardiovascular and inflammatory biomarkers in paediatric dengue shock syndrome","authors":"Chanh Ho Quang, Trieu Huynh Trung, Tam Dong Thi Hoai, Tran Kim Hung, Huynh Ngoc Thien Vuong, Phan Tu Qui, Huyen Vu Ngo Thanh, Alexandra Moncada, Thanh Kieu Nguyen Thi, Duyen Huynh Thi Le, Ngan Nguyen-Lyle, Vuong Nguyen Lam, Lam Phung Khanh, Angela McBride, Bridget Wills, Sophie Yacoub","doi":"10.1093/oxfimm/iqae005","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae005","url":null,"abstract":"\u0000 \u0000 \u0000 Glycocalyx disruption and hyperinflammatory responses are implicated in the pathogenesis of dengue-associated vascular leak, however little is known about their association with clinical outcomes of patients with dengue shock syndrome (DSS). We investigated the association of vascular and inflammatory biomarkers with clinical outcomes and their correlations with clinical markers of vascular leakage.\u0000 \u0000 \u0000 \u0000 We performed a prospective cohort study in Viet Nam. Children ≥ 5 years of age with a clinical diagnosis of DSS were enrolled into this study. Blood samples were taken daily during ICU stay and 7–10 days after hospital discharge for measurements of plasma levels of Syndecan-1, Hyaluronan, Suppression of tumorigenicity 2 (ST-2), Ferritin, N-terminal pro Brain Natriuretic Peptide (NT-proBNP), and Atrial Natriuretic Peptide (ANP). The primary outcome was recurrent shock.\u0000 \u0000 \u0000 \u0000 90 DSS patients were enrolled. Recurrent shock occurred in 16 patients. All biomarkers, except NT-proBNP, were elevated at presentation with shock. There were no differences between compensated and decompensated DSS patients. Glycocalyx markers were positively correlated with inflammatory biomarkers, haematocrit, percentage hemoconcentration, and negatively correlated with stroke volume index. While Syndecan-1, Hyaluronan, Ferritin, and ST-2 improved with time, ANP continued to be raised at follow-up. Enrolment Syndecan-1 levels were observed to be associated with developing recurrent shock although the association did not reach the statistical significance at the P < 0.01 (OR = 1.82, 95% CI 1.07–3.35, P = 0.038).\u0000 \u0000 \u0000 \u0000 Cardiovascular and inflammatory biomarkers are elevated in DSS, correlate with clinical vascular leakage parameters and follow different kinetics over time. Syndecan-1 may have potential utility in risk stratifying DSS patients in ICU.\u0000","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"29 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141271590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
David Guerrero, Sokchea Lay, E. Piv, Chansophea Chhin, Sokkeang Leng, Ratana Meng, Kim Eng Mam, P. Pean, Amelie Vantaux, Sebastien Boyer, Dorothée Missé, T. Cantaert
{"title":"In-Vitro assessment of cutaneous immune responses to aedes mosquito salivary gland extract and dengue virus in cambodian individuals","authors":"David Guerrero, Sokchea Lay, E. Piv, Chansophea Chhin, Sokkeang Leng, Ratana Meng, Kim Eng Mam, P. Pean, Amelie Vantaux, Sebastien Boyer, Dorothée Missé, T. Cantaert","doi":"10.1093/oxfimm/iqae003","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae003","url":null,"abstract":"\u0000 Dengue virus (DENV) poses a global health threat, affecting millions annually with no specific therapy and limited vaccines. Mosquitoes, mainly Aedes aegypti and Aedes albopictus worldwide, transmit DENV through their saliva during blood meals. In this study, we aimed to understand how Aedes mosquito saliva modulate skin immune responses during DENV infection in individuals living in mosquito-endemic regions. To accomplish this, we dissociated skin cells from Cambodian volunteers and incubated them with salivary gland extract (SGE) from 3 different mosquito strains: Ae. aegypti USDA strain, Ae. aegypti and Ae. albopictus wild type (WT) in the presence/absence of DENV.\u0000 We observed notable alterations in immune skin cells phenotypes subsequent to exposure to Aedes salivary gland extract (SGE). Specifically, exposure lead to an increase in the frequency of macrophages expressing chemokine receptor CCR2, and neutrophils expressing CD69. Additionally, we noted a substantial increase in the percentage of macrophages that became infected with DENV in the presence of Aedes SGE. Differences in cellular responses were observed when Aedes SGE of three distinct mosquito strains were compared.\u0000 Our findings deepen the understanding of mosquito saliva's role in DENV infection and skin immune responses in individuals regularly exposed to mosquito bites. This study provides insights into skin immune cell dynamics that could guide strategies to mitigate DENV transmission and other arbovirus diseases.","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"468 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140759597","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tohnyui Ndinyanka Fabrice, Mayumi Mori, Jean Pieters
{"title":"Coronin 1-dependent cell density sensing and regulation of the peripheral T cell population size","authors":"Tohnyui Ndinyanka Fabrice, Mayumi Mori, Jean Pieters","doi":"10.1093/oxfimm/iqae002","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae002","url":null,"abstract":"\u0000 The establishment and maintenance of peripheral T cells is important to ensure appropriate immunity. In mammals, T cells are produced in the thymus before seeding the periphery early in life, and thereafter progressive thymus involution impairs new T cell production. Yet, peripheral T cells are maintained lifelong at approximately similar cell numbers. The question thus arises: what are the mechanisms that enable the maintenance of the appropriate number of circulating T cells, ensuring that T cell numbers are neither too low nor too high? Here, we highlight recent research suggesting a key role for coronin 1, a member of the evolutionarily conserved family of coronin proteins, in both allowing T cells to reach as well as maintain their appropriate cell population size. This cell population size controlling pathway was found to be conserved in amoeba, mice and human. We propose that coronin 1 is an integral part of a cell-intrinsic pathway that couples cell density information with prosurvival signalling thereby regulating the appropriate number of peripheral T cells.","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":" 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140217798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sthembile Mbotwe-Sibanda, G. Kwatra, S. Madhi, Marta C. Nunes
{"title":"Post-acute sequelae of SARS-CoV-2 infection in health care workers from South Africa","authors":"Sthembile Mbotwe-Sibanda, G. Kwatra, S. Madhi, Marta C. Nunes","doi":"10.1093/oxfimm/iqae001","DOIUrl":"https://doi.org/10.1093/oxfimm/iqae001","url":null,"abstract":"\u0000 Health care workers (HCWs) are primary health providers therefore ensuring their protection and recovery from Covid-19 is of high interest. We investigated post-acute sequelae of SARS-CoV-2 infection (PASC) in HCWs who had previously been infected with SARS-CoV-2. Overall, 68 HCWs were classified as PASC according to duration in days of persisting symptoms. The 68 HCWs with PASC were split into two groups according to their mean duration of symptoms which were (8 PASC) 122 and (60 PASC) 641 days. The frequencies of common symptoms reported by HWCs with PASC were continuous headaches (45), mild cough (41), fatigue (37), myalgia (25) and shortness of breath (14). When Using the Medical Research Council (MRC) Dyspnoea Scale to examine the degree of breathlessness in relations to activity in the 68 out of the 104 HCWs with PASC we found that 4 (5.9%) reported having difficulty breathing after strenuous exercise, 19 (27.9%) were identified with shortness of breath when walking fast or when walking up a slight hill, 2 (3.0%) reported walking slower than most people on level or stopping after 15 minutes walking at own pace, 1 (1.5%) reported stopping to breath after walking 91 meters, or after a few minutes on level ground and 1 (1.5%) reported being too breathless to leave the house, or breathless when dressing/undressing. Our results highlight concern for HCWs with long-term persisting symptoms which may negatively impact their health this represents an emerging public health priority. HCWs with prolonged Covid-19 symptoms especially breathing difficulties need better diagnostic tests and treatments.","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"146 S282","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140256634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Oxford open immunologyPub Date : 2023-11-15eCollection Date: 2023-01-01DOI: 10.1093/oxfimm/iqad008
Else M Bijker, Sanjay Deshpande, Padmini Salgame, Rinn Song
{"title":"Malaria and tuberculosis co-infection-a review.","authors":"Else M Bijker, Sanjay Deshpande, Padmini Salgame, Rinn Song","doi":"10.1093/oxfimm/iqad008","DOIUrl":"https://doi.org/10.1093/oxfimm/iqad008","url":null,"abstract":"<p><p>Malaria and tuberculosis remain highly prevalent infectious diseases and continue to cause significant burden worldwide. Endemic regions largely overlap, and co-infections are expected to occur frequently. Surprisingly, malaria-tuberculosis co-infection is relatively understudied. Malaria has long been known to have immunomodulatory effects, for example resulting in reduced vaccination responses against some pathogens, and it is conceivable that this also plays a role if co-infection occurs. Data from animal studies indeed suggest clinically important effects of malaria-tuberculosis co-infection on the immune responses with potential consequences for the pathophysiology and clinical course of both infections. Specifically, rodent studies consistently show reduced control of mycobacteria during malaria infection. Although the underlying immunological mechanisms largely remain unclear, an altered balance between pro- and anti-inflammatory responses may play a role. Some observations in humans also support the hypothesis that malaria infection skews the immune responses against tuberculosis, but data are limited. Further research is needed to unravel the underlying immunological mechanisms and delineate possible implications of malaria-tuberculosis co-infection for clinical practice.</p>","PeriodicalId":74384,"journal":{"name":"Oxford open immunology","volume":"4 1","pages":"iqad008"},"PeriodicalIF":0.0,"publicationDate":"2023-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10681873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138813565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}