Phenotyping the host immune response to infection: the critical role of biomarkers in sepsis

2021 ◽  
Author(s):  
Salvatore L. CUTULI ◽  
Simone CARELLI ◽  
Gennaro DE PASCALE
Keyword(s):  
Immune Response ◽  
Critical Role ◽  
Host Immune Response

COVID-19: Inflammatory Profile

2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Yuhang Wang ◽  
Stanley Perlman
Keyword(s):  
Immune Response ◽  
Distress Syndrome ◽  
Multiorgan Failure ◽  
Critical Role ◽  
Host Immune Response ◽  
Immune Dysregulation ◽  
Annual Review ◽  
Publication Date ◽  
Inflammatory Profile

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), has resulted in a pandemic that has had widespread effects on human activities. The clinical presentation of severe COVID-19 includes a broad spectrum of clinical disease, most notably acute respiratory distress syndrome, cytokine release syndrome (CRS), multiorgan failure, and death. Direct viral damage and uncontrolled inflammation have been suggested as contributory factors in COVID-19 disease severity. The COVID-19 pandemic has emphasized the critical role of an effective host immune response in controlling a virus infection and demonstrated the devastating effect of immune dysregulation. Understanding the nature of the immune response to SARS-CoV-2 pathogenesis is key to developing effective treatments for COVID-19. Here, we describe the nature of the dysregulated host immune response in COVID-19, identify potential mechanisms involved in CRS, and discuss potential strategies that can be used to manage immune dysregulation in COVID-19. Expected final online publication date for the Annual Review of Medicine, Volume 73 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

scholarly journals NLRP7 Promotes Choriocarcinoma Growth and Progression through the Establishment of an Immunosuppressive Microenvironment

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2999
Author(s):  
Deborah Reynaud ◽  
Roland Abi Nahed ◽  
Nicolas Lemaitre ◽  
Pierre-Adrien Bolze ◽  
Wael Traboulsi ◽  
...  
Keyword(s):  
Immune Response ◽  
Tumor Cells ◽  
Major Gene ◽  
Critical Role ◽  
Orthotopic Model ◽  
Independent Manner ◽  
Maternal Immune Response ◽  
The Impact

The inflammatory gene NLRP7 is the major gene responsible for recurrent complete hydatidiform moles (CHM), an abnormal pregnancy that can develop into gestational choriocarcinoma (CC). However, the role of NLRP7 in the development and immune tolerance of CC has not been investigated. Three approaches were employed to define the role of NLRP7 in CC development: (i) a clinical study that analyzed human placenta and sera collected from women with normal pregnancies, CHM or CC; (ii) an in vitro study that investigated the impact of NLRP7 knockdown on tumor growth and organization; and (iii) an in vivo study that used two CC mouse models, including an orthotopic model. NLRP7 and circulating inflammatory cytokines were upregulated in tumor cells and in CHM and CC. In tumor cells, NLRP7 functions in an inflammasome-independent manner and promoted their proliferation and 3D organization. Gravid mice placentas injected with CC cells invalidated for NLRP7, exhibited higher maternal immune response, developed smaller tumors, and displayed less metastases. Our data characterized the critical role of NLRP7 in CC and provided evidence of its contribution to the development of an immunosuppressive maternal microenvironment that not only downregulates the maternal immune response but also fosters the growth and progression of CC.

The possible role of the frontal and sub-parietal gland systems of the pentastomidReighardia sternae(Diesing, 1864) in the evasion of the host immune response

Parasitology ◽  
1979 ◽  
Vol 78 (1) ◽  
pp. 53-66 ◽  
Author(s):  
J. Riley ◽  
J. L. James ◽  
A. A. Banaja
Keyword(s):  
Immune Response ◽  
Alternative Explanation ◽  
Surface Membrane ◽  
Membrane System ◽  
Host Immune Response ◽  
Entire Surface ◽  
Strong Immune Response ◽  
Concomitant Immunity ◽  
Host Parasite

SUMMARYThe frontal and sub-parietal glands of the pentastomidReighardia sternaeelaborate lamellate secretion which is poured on to the cuticle. The entire surface of the cuticle, including the mouth, hook pits and reproductive apertures, is coated with secretion. Electron microscope studies indicate that the glands are continuously active, which implies a turnover of surface membranes. The postulated function of these membranes is to protect certain vital areas of the host–parasite interface, notably the pores of ion-transporting cells, from the host immune response. The available evidence suggests that pentastomids do evoke a strong immune response but since most are long-lived they must circumvent it. We believe the surface membrane system to be instrumental in this. Studies on another pentastomid,Porocephalus crotaliin rats have shown that an immune response stimulated by a primary infection will kill subsequent infections and that the surface membranes are strongly immunogenic. Obvious parallels between this situation and that of schistosome infections in mammals are discussed. An alternative explanation of concomitant immunity is proposed.

scholarly journals Immunity and its role in periodontal diseases

2017 ◽  
Vol 63 (1) ◽  
pp. 24-27
Author(s):  
Irina Dumitrache ◽  
Keyword(s):  
Immune Response ◽  
Chronic Disease ◽  
Periodontal Disease ◽  
Clinical Efficacy ◽  
Periodontal Diseases ◽  
Adult Population ◽  
Host Immune Response ◽  
Immunomodulatory Therapy ◽  
Common Chronic Disease

Periodontal disease is one of the most common chronic disease, with a prevalence between 5% and 30% in adult population aged 25-75. In the pathogenesis of periodontal disease, the host immune response has a great importance and in the last years it has been underlined the role of immunomodulatory therapy in the management of periodontal disease. Septilin is a herbal immunomodulatory with clinical efficacy proven in the periodontal disease.

scholarly journals Role of Host Immune Response and Viral Load in the Differential Outcome of Pandemic H1N1 (2009) Influenza Virus Infection in Indian Patients

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13099 ◽  
Author(s):  
Vidya A. Arankalle ◽  
Kavita S. Lole ◽  
Ravi P. Arya ◽  
Anuradha S. Tripathy ◽  
Ashwini Y. Ramdasi ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Viral Load ◽  
Virus Infection ◽  
Influenza Virus Infection ◽  
Host Immune Response ◽  
Pandemic H1n1 ◽  
Differential Outcome ◽  
Pandemic H1n1 2009

Role of DNA repair in host immune response and inflammation

2015 ◽  
Vol 763 ◽  
pp. 246-257 ◽  
Author(s):  
Fabrícia Lima Fontes ◽  
Daniele Maria Lopes Pinheiro ◽  
Ana Helena Sales de Oliveira ◽  
Rayssa Karla de Medeiros Oliveira ◽  
Tirzah Braz Petta Lajus ◽  
...  
Keyword(s):  
Immune Response ◽  
Dna Repair ◽  
Host Immune Response

scholarly journals Review on the Role of Host Immune Response in Protection and Immunopathogenesis during Cutaneous Leishmaniasis Infection

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Teshager Dubie ◽  
Yasin Mohammed
Keyword(s):  
Immune Response ◽  
Cutaneous Leishmaniasis ◽  
Proinflammatory Cytokines ◽  
Parasitic Infection ◽  
Host Immune Response ◽  
Immune Defense ◽  
Host Cells ◽  
Infected Host ◽  
Major Public Health Problem

Cutaneous leishmaniasis (CL) is a major public health problem worldwide and spreads to human via the bite of sand flies during blood meal. Following its inoculation, the promastigotes are immediately taken up by phagocytic cells and these leishmania-infected host cells produce proinflammatory cytokines that activate other immune cells and these infected host cells produce more cytokines and reactive nitrogen and oxygen species for efficient control of leishmania infection. Many experimental studies showed that resistance to infection with leishmania paraites is associated with the production of proinflammatory cytokines and activation of CD4+ Th1 response. On the other hand, vulnerability to this parasitic infection is correlated to production of T helper 2 cytokines that facilitate persistence of parasites and disease progression. In addition, some studies have also indicated that CD8+ T cells play a vital role in immune defense through cytokine production and their cytotoxic activity and excessive production of proinflammatory mediators promote amplified recruitment of cells. This could be correlated with excessive inflammatory reaction and ultimately resulted in tissue destruction and development of immunopathogenesis. Thus, there are contradictions regarding the role of immune responses in protection and immunopathogenesis of CL disease. Therefore, the aim of this paper was to review the role of host immune response in protection and its contribution to disease severity for CL infection. In order to obtain more meaningful data regarding the nature of immune response to leishmania, further in-depth studies focused on immune modulation should be conducted to develop better therapeutic strategies.

8 ROLE OF THE HOST IMMUNE RESPONSE TO ENTERIC PROKARYOTIC VIRUSES IN INFLAMMATORY BOWEL DISEASE

2020 ◽  
Vol 158 (3) ◽  
pp. S68-S69
Author(s):  
Julia Angkeow ◽  
Daniel Monaco ◽  
Scott Handley ◽  
H.B. Larman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune Response ◽  
Bowel Disease ◽  
Host Immune Response ◽  
Inflammatory Bowel

scholarly journals Crosstalk between Dendritic Cells and Immune Modulatory Agents against Sepsis

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 323 ◽  
Author(s):  
Guoying Wang ◽  
Xianghui Li ◽  
Lei Zhang ◽  
Abualgasim Elgaili Abdalla ◽  
Tieshan Teng ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Critical Role ◽  
Innate Immune ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Th2 Responses ◽  
Novel Strategy

Dendritic cells (DCs) play a critical role in the immune system which sense pathogens and present their antigens to prime the adaptive immune responses. As the progression of sepsis occurs, DCs are capable of orchestrating the aberrant innate immune response by sustaining the Th1/Th2 responses that are essential for host survival. Hence, an in-depth understanding of the characteristics of DCs would have a beneficial effect in overcoming the obstacle occurring in sepsis. This paper focuses on the role of DCs in the progression of sepsis and we also discuss the reverse sepsis-induced immunosuppression through manipulating the DC function. In addition, we highlight some potent immunotherapies that could be used as a novel strategy in the early treatment of sepsis.

scholarly journals Toll-like receptor 9 inhibition reduces mortality in polymicrobial sepsis

2008 ◽  
Vol 205 (6) ◽  
pp. 1277-1283 ◽  
Author(s):  
George Plitas ◽  
Bryan M. Burt ◽  
Hoang M. Nguyen ◽  
Zubin M. Bamboat ◽  
Ronald P. DeMatteo
Keyword(s):  
Immune Response ◽  
Critical Role ◽  
Cecal Ligation ◽  
High Rate ◽  
Microbial Pathogens ◽  
Lower Serum ◽  
Human Sepsis ◽  
Cytokine Levels ◽  
Potential Strategy

The high rate of mortality in patients with sepsis results from an inappropriately amplified systemic inflammatory response to infection. Toll-like receptors (TLRs) are important for the activation of innate immunity against microbial pathogens. We demonstrate a critical role of TLR9 in the dysregulated immune response and death associated with sepsis. Compared with wild-type (WT) mice, TLR9−/− mice exhibited lower serum inflammatory cytokine levels, higher bacterial clearance, and greater survival after experimental peritonitis induced by cecal ligation and puncture (CLP). Protection of TLR9−/− mice after CLP was associated with a greater number of peritoneal dendritic cells (DCs) and granulocytes than in WT controls. Adoptive transfer of TLR9−/− DCs was sufficient to protect WT mice from CLP and increased the influx of peritoneal granulocytes. Subsequent experiments with a depleting antibody revealed that granulocytes were required for survival in TLR9−/− mice. Remarkably, a single injection of an inhibitory CpG sequence that blocks TLR9 protected WT mice, even when administered as late as 12 h after CLP. Our findings demonstrate that the detrimental immune response to bacterial sepsis occurs via TLR9 stimulation. TLR9 blockade is a potential strategy for the treatment of human sepsis.

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