Polycystic ovary syndrome and its management: In view of oxidative stress.

In the past two decades, oxidative stress (OS) has drawn a lot of interest due to the revelation that individuals with many persistent disorders including diabetes, polycystic ovarian syndrome (PCOS), cardiovascular, and other disorders often have aberrant oxidation statuses. OS has a close interplay with PCOS features such as insulin resistance, hyperandrogenism, and chronic inflammation; there is a belief that OS might contribute to the development of PCOS. PCOS is currently recognized as not only one of the most prevalent endocrine disorders but also a significant contributor to female infertility, affecting a considerable proportion of women globally.

Microglial Inflammatory Responses to SARS-CoV-2 Infection: A Comprehensive Review.

Coronavirus disease 2019 (COVID-19) is primarily a respiratory disease causing a worldwide pandemic in the year of 2019. SARS-CoV-2 is an enveloped, positive-stranded RNA virus that could invade the host through spike protein and exhibits multi-organ effects. The Brain was considered to be a potential target for SARS-CoV-2 infection.

Exogenous IL-10 posttreatment along with TLR4 and TNFR1 blockade improves tissue antioxidant status by modulating sepsis-induced macrophage polarization.

Multi-organ dysfunction is one of the major reasons behind the high mortality of sepsis throughout the world. With the pathophysiology of sepsis remaining largely unknown, the uncontrolled reactive oxygen species (ROS) production along with the decreased antioxidants contributes to the progression toward septic shock. Being the effector cells of the innate immunity system, macrophages secrete both pro-inflammatory and anti-inflammatory mediators during inflammation.

Synovial macrophages of rheumatoid arthritic mice protectively responded by altered M1/M2 differentiation after antibody blocking of TNFR1 and IL-1R.

Rheumatoid arthritis (RA) primarily affecting the synovial tissue, has emerged as a major concern leading to the pressing need to develop effective treatment strategies. In the affected synovial tissue, resident macrophages play a pivotal role in the pathogenesis of RA. TNF-α and IL-1β released from pro-inflammatory M1 synovial macrophages are the master regulators of chronic joint inflammation.

Simultaneous neutralization of TGF-β and IL-6 attenuates Staphylococcus aureus-induced arthritic inflammation through differential modulation of splenic and synovial macrophages.

Septic arthritis is a joint disease caused by Staphylococcus aureus. Different macrophage populations contribute in various ways to control blood-borne infections and induce inflammatory responses. Macrophage tissue-resident niche is necessary for the suppression of chronic inflammation and may contribute to the pathogenesis of septic arthritis.

Endogenous neutralization of TGF-β and IL-6 ameliorates septic arthritis by altering RANKL/OPG interaction in lymphocytes.

Septic arthritis is an inflammatory joint disease caused by S. aureus. Hematogenous entry of the bacteria to the synovium produces pro-inflammatory cytokines TGF-β and IL-6, which alter the Th17/Treg balance.

Ascorbic acid along with ciprofloxacin regulates S. aureus induced microglial inflammatory responses and oxidative stress through TLR-2 and glucocorticoid receptor modulation.

Microglial inflammatory responses play a central role in the pathogenesis of S. aureus induced brain infections. Upon activation, microglia produces free radicals (ROS/RNS) and disrupts the cellular antioxidant defense to combat invading microorganisms.

Neutralization of IL-17 and treatment with IL-2 protects septic arthritis by regulating free radical production and antioxidant enzymes in Th17 and Tregs: An immunomodulatory TLR2 versus TNFR response.

Septic arthritis is a destructive joint disease caused by Staphylococcus aureus. Synovial inflammation involved Th17 proliferation and down regulation of Treg population, thus resolution of inflammation targeting IL-17 may be important to control arthritis. Endogenous inhibition of IL-17 to regulate arthritic inflammation correlating with Th17/Treg cells TLR2 and TNFRs are not done.

TLR4 and TNFR1 blockade dampen M1 macrophage activation and shifts them towards an M2 phenotype.

The Gram-negative bacterial lipopolysaccharide (LPS)-induced sepsis has emerged as major concern worldwide due to the pressing need to develop its effective treatment strategies which is not available yet. LPS is the major causative agent in the pathogenesis of septic shock. In macrophages, LPS interacts with cell surface TLR4 leading to reactive oxygen species (ROS), TNF-α, IL-1β production, oxidative stress and markedly activated the MAPKs and NF-kB pathway.

Ciprofloxacin and dexamethasone in combination attenuate S. aureus induced brain abscess via neuroendocrine-immune interaction of TLR-2 and glucocorticoid receptor leading to behavioral improvement.

Staphylococcus aureus induced brain abscess is a critical health concern throughout the developing world. The conventional surgical intervention could not regulate the abscess-induced brain inflammation. Thus further study over the alternative therapeutic strategy for treating a brain abscess is of high priority.

TLR-2 neutralization potentiates microglial M1 to M2 switching by the combinatorial treatment of ciprofloxacin and dexamethasone during S. aureus infection.

Microglial inflammation plays a pivotal role in the pathogenesis of S. aureus induced brain abscesses. The objective of this study was to regulate microglial activation by the combinatorial treatment of ciprofloxacin either with dexamethasone or celecoxib via targeting M1 and M2 polarization.

Dexamethasone along with ciprofloxacin modulates S. aureus induced microglial inflammation via glucocorticoid (GC)-GC receptor-mediated pathway.

Microglial inflammation is the hallmark of S. aureus induced brain abscesses. Conventional antibiotic therapy could not regulate inflammation and the use of steroids in CNS infection remained controversial.

Dexamethasone exhibits its anti-inflammatory effects in S. aureus induced microglial inflammation via modulating TLR-2 and glucocorticoid receptor expression.

Microglial inflammation plays crucial role in the pathogenesis of CNS infections including brain abscesses. Staphylococcus aureus (S. aureus) is considered as one of the major causative agents of brain abscesses.

Regulation of Staphylococcus aureus-induced CXCR1 expression via inhibition of receptor mobilization and receptor shedding during dual receptor (TNFR1 and IL-1R) neutralization.

Our earlier studies proposed a radically new idea suggesting interdependency between TNF-α/TNFR1 and IL-1β/IL-1R pathways in modulation of Staphylococcus aureus-induced CXCL8/CXCR1 axis. However, the effects of inhibition of cytokine receptor mobilization at intracellular level and surface TNFR1 and IL-1R shedding on S. aureus-induced CXCR1 expression have not been studied so far in peritoneal macrophages.

Role of plasminogen activator inhibitor - 1 (PAI-1) in regulating the pathogenesis of S. aureus arthritis via plasminogen pathway.

uPA/tPA-mediated activation of plasminogen/plasmin pathway during S. aureus arthritis facilitates the invasion of phagocytes in the affected joint, induces production of cytokines and triggers inflammatory pathways. PAI-1, an effective inhibitor of both uPA and tPA, attenuates plasmin activity.

Combination treatment of celecoxib and ciprofloxacin attenuates live S. aureus induced oxidative damage and inflammation in murine microglia via regulation of cytokine balance.

Microglial activation is the most common phenomenon in S. aureus induced brain abscesses as well as other common neurodegenerative diseases. The main objective of this study is to reduce the microglial inflammation with effective bacterial elimination.

Dual neutralization of TNFR-2 and MMP-2 regulates the severity of S. aureus induced septic arthritis correlating alteration in the level of interferon gamma and interleukin-10 in terms of TNFR2 blocking.

Severity of S. aureus septic arthritis is correlated to prolonged inflammation by inflammatory cytokines like TNF-α, IL-1β, and IL-6 even after successful elimination of bacteria. Role of TNF-α via TNFR2 is not well established in this aspect.

Altered expression of CXCR1 (IL-8R) in macrophages utilizing cell surface TNFR1 and IL-1 receptor during Staphylococcus aureus infection.

Currently, very few studies are available on the expression of CXCR1 in mouse macrophages having both intact TNFR1 and IL-1R or their deficiency in relation to acute S. aureus infection. Peritoneal macrophages from mice neutralized singly for TNFR1or IL-1R, or for both TNFR1 and IL-1R were infected with S.

Expression of CXCR1 (IL-8 receptor A) in splenic, peritoneal macrophages and resident bone marrow cells after acute live or heat killed Staphylococcus aureus stimulation in mice.

Literature reveals that interaction with live Staphylococcus aureus (S. aureus) or heat killed S. aureus (HKSA) promotes secretion of CXCL-8 or interleukin-8 (IL-8) from leukocytes, however, the expressions of CXCR1 in murine splenic (SPM), peritoneal macrophages (PM) and resident fresh bone marrow cells (FBMC) have not been identified.