Evidence for a Gender-Specific Protective Role of Innate Immune Receptors in a Model of Perinatal Brain Injury

Oxidative stress contributes to the severity of several newborn conditions to the extent that Saugstad coined the phrase “oxygen radical diseases of neonatology.” In order to counteract free radicals damage many strategies to augment antioxidant status in ill-term and preterm infants have been proposed and several medications have been experimented with mixed results. Several studies have tested the efficacy of melatonin to counteract oxidative damage in diseases of newborns such as chronic lung disease, perinatal brain injury, necrotizing enterocolitis, and retinopathy of prematurity, giving promising results. The peculiar perinatal susceptibility to oxidative stress indicates that prophylactic use of antioxidants as melatonin could help to prevent or at least reduce oxidative stress related diseases in newborns. However, more studies are needed to confirm these beneficial effects.

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Update on the role of innate immune receptors during Brucella abortus infection

Veterinary Immunology and Immunopathology ◽

10.1016/j.vetimm.2011.05.036 ◽

2012 ◽

Vol 148 (1-2) ◽

pp. 129-135 ◽

Cited By ~ 17

Author(s):

Sérgio C. Oliveira ◽

Leonardo A. de Almeida ◽

Natalia B. Carvalho ◽

Fernanda S. Oliveira ◽

Thaís L.S. Lacerda

Keyword(s):

Brucella Abortus ◽

Innate Immune ◽

Immune Receptors

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Protective Role of Apocynin via Suppression of Neuronal Autophagy and TLR4/NF-κB Signaling Pathway in a Rat Model of Traumatic Brain Injury

Neurochemical Research ◽

10.1007/s11064-017-2372-z ◽

2017 ◽

Vol 42 (11) ◽

pp. 3296-3309 ◽

Cited By ~ 18

Author(s):

Yan Feng ◽

Changmeng Cui ◽

Xin Liu ◽

Qiang Wu ◽

Fuguang Hu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Signaling Pathway ◽

Rat Model ◽

Protective Role ◽

Neuronal Autophagy

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Ischemic brain injury: New insights on the protective role of melatonin

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2017.01.005 ◽

2017 ◽

Vol 104 ◽

pp. 32-53 ◽

Cited By ~ 45

Author(s):

Eva Ramos ◽

Paloma Patiño ◽

Russel J. Reiter ◽

Emilio Gil-Martín ◽

José Marco-Contelles ◽

...

Keyword(s):

Brain Injury ◽

Protective Role ◽

Ischemic Brain Injury ◽

Ischemic Brain

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The Innate Immune Receptor CD14 Mediates Lymphocyte Migration in EAE

Cellular Physiology and Biochemistry ◽

10.1159/000430351 ◽

2015 ◽

Vol 37 (1) ◽

pp. 269-275 ◽

Cited By ~ 6

Author(s):

Ramona Halmer ◽

Laura Davies ◽

Yang Liu ◽

Klaus Fassbender ◽

Silke Walter

Keyword(s):

Multiple Sclerosis ◽

T Cell ◽

Experimental Autoimmune Encephalomyelitis ◽

T Cell Activation ◽

Cell Activation ◽

Innate Immune ◽

Autoimmune Encephalomyelitis ◽

Immune Receptors ◽

Experimental Autoimmune

Background: Multiple sclerosis is the most common autoimmune disease of the central nervous system in young adults and histopathologically characterized by inflammation, demyelination and gliosis. It is considered as a CD4+ T cell-mediated disease, but also a disease-promoting role of the innate immune system has been proposed, based e.g. on the observation that innate immune receptors modulate disease severity of experimental autoimmune encephalomyelitis. Recent studies of our group provided first evidence for a key role of the innate immune LPS receptor (CD14) in pathophysiology of experimental autoimmune encephalomyelitis. CD14-deficient experimental autoimmune encephalomyelitis mice showed increased clinical symptoms and enhanced infiltration of monocytes and neutrophils in brain and spinal cord. Methods: In the current study, we further investigated the causes of the disease aggravation by CD14-deficiency and examined T cell activation, also focusing on the costimulatory molecules CTLA-4 and CD28, and T cell migration capacity over the blood brain barrier by FACS analysis, in vitro adhesion and transmigration assays. Results: In the results, we observed a significantly increased migration of CD14-deficient lymphocytes across an endothelial monolayer. In contrast, we did not see any differences in expression levels of TCR/CTLA-4 or TCR/CD28 and lymphocyte adhesion to endothelial cells from CD14-deficient compared to wildtype mice. Conclusion: The results demonstrate an important role of CD14 in migration of lymphocytes, and strengthen the importance of innate immune receptors in adaptive immune disorders, such as multiple sclerosis.

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New Insights on the Role of pentraxin-3 in Allergic Asthma

Frontiers in Allergy ◽

10.3389/falgy.2021.678023 ◽

2021 ◽

Vol 2 ◽

Author(s):

Latifa Koussih ◽

Samira Atoui ◽

Omar Tliba ◽

Abdelilah S. Gounni

Keyword(s):

Immune Response ◽

Allergic Asthma ◽

Current Knowledge ◽

Inflammatory Diseases ◽

Protective Role ◽

Severe Form ◽

Innate Immune ◽

Pentraxin 3 ◽

Complement Components

Pentraxins are soluble pattern recognition receptors that play a major role in regulating innate immune responses. Through their interaction with complement components, Fcγ receptors, and different microbial moieties, Pentraxins cause an amplification of the inflammatory response. Pentraxin-3 is of particular interest since it was identified as a biomarker for several immune-pathological diseases. In allergic asthma, pentraxin-3 is produced by immune and structural cells and is up-regulated by pro-asthmatic cytokines such as TNFα and IL-1β. Strikingly, some recent experimental evidence demonstrated a protective role of pentraxin-3 in chronic airway inflammatory diseases such as allergic asthma. Indeed, reduced pentraxin-3 levels have been associated with neutrophilic inflammation, Th17 immune response, insensitivity to standard therapeutics and a severe form of the disease. In this review, we will summarize the current knowledge of the role of pentraxin-3 in innate immune response and discuss the protective role of pentraxin-3 in allergic asthma.

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Trem-2 modulation of gut microbiota is blunted during hepatotoxic injury and uncoupled from liver repair responses

10.1101/857078 ◽

2019 ◽

Author(s):

Inês Coelho ◽

Nádia Duarte ◽

Maria Paula Macedo ◽

Carlos Penha-Gonçalves

Keyword(s):

Gut Microbiota ◽

Liver Damage ◽

Liver Tissue ◽

Innate Immune ◽

Microbiota Composition ◽

Wild Type ◽

Immune Receptors ◽

Microbiota Diversity ◽

Gut Microbiota Composition

AbstractThe involvement of gut microbiota in liver disease has been addressed in the context of the “leaky gut hypothesis” postulating that dysbiosis allow microbial components to elicit liver inflammatory responses and hepatic tissue damage. Conversely, commensal gut microbiota acting on innate immune receptors protect against hepatotoxic insults. Given that mice deficient for the triggering receptor expressed on myeloid cells-2 (Trem-2) show increased vulnerability to experimental drug-induced hepatic damage we explored the possibility that Trem-2 is a modulator of gut microbiota composition.We found that microbiota composition in untreated Trem-2 KO mice differs from the wild-type showing overall decrease in microbiota diversity and increased representation of Verrucomicrobia. Interestingly, induction of liver damage with hepatotoxic drugs blunted this microbiota diversity difference and altered phyla composition with increased representation of Verrucomicrobia during acute hepatic injury and Proteobacteria during chronic challenge. Furthermore, co-housing experiments that homogenized microbiota diversity showed that the increased liver tissue vulnerability to hepatotoxic insults in Trem-2 KO mice was not dependent on microbiota composition. This work uncouples Trem-2 dependent alterations in gut commensal microbiota from Trem-2 pro-recovery effects in the damaged liver tissue. These findings support the possibility that unlinked actions of innate immune receptors contribute to disease association with microbiota alterations, particularly with the Verrucomicrobia phylum.ImportanceTrem-2 is a mammalian innate immunity receptor involved in development and resolution of tissue damage, namely in the brain and in the liver. Nevertheless, it is not known whether gut microbiota is contributing to these Trem-2 mediated phenotypes. We found that Trem-2 KO mice spontaneously display different gut microbiota composition as compared to wild-type mice, namely with increased abundance of the phylum Verrucomicrobia. Notably these differences do not impact the control of Trem-2 on liver tissue vulnerability to hepatotoxic insults. This work uncouples Trem-2 modulation of gut microbiota and the role of Trem-2 on responses to liver damage. This work brings new insights on role of innate immune receptors on the association of organic and systemic diseases with gut microbiota.

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