Chloramphenicol is mostly used against coagulase-negative Staphylococcus aureus, and its protective role against coagulase-positive S. aureus is not well studied. In our study, arthritis was induced in mice by S. aureus (Apollo Gleneagles 33 (AG-33) or American Type Culture Collection 25923 (ATCC-25923)) infection. Chloramphenicol was administered after 2 h of infection. Mice were killed at 1, 3, 5 days post-infection. Mice inoculated with pathogenic Staphylococci (AG-33) expressing coagulase and Toxic shock syndrome toxin-1 (TSST-1), displayed severe arthritis with enhanced bacterial burden in the spleen, cytokine production in serum and synovial tissue, neutrophil recruitment, and cyclooxegenase-2 expression in synovial tissue compared with ATCC-25923-infected groups. Severity of arthritis was regulated by chloramphenicol treatment. Our study suggests that alteration in the inflammatory cytokine levels and pronounced production of cyclooxygenase-2 play important roles in progression of arthritis which is regulated by application of chloramphenicol. © 2010 Springer Science+Business Media, LLC.

BISWADEV BISHAYI

Physiology

S MAJUMDAR

K DUTTA

S K MANNA

A BASU

University of Calcutta (informally known as Calcutta University or CU) is a collegiate public state university located in Kolkata, West Bengal, India.&nbsp;Within India it is recognized as a &quot;Five-Star University&quot; and accredited &quot;A&quot; Grade by National Assessment and Accreditation Council.

&nbsp;

The University of Calcutta has secured the Fifth position among the Universities of India in the prestigious &quot;Indian University Ranking 2019&quot; list, released by the NIRF of the Ministry of Human Resource Development, Government of India.

&nbsp;

It was established on 24 January 1857, and was one of the first institutions in Asia to be established as a multidisciplinary and Western-style university. Its alumni and faculty include several heads of state, heads of government, social reformers, prominent artists, only academy award winner and Dirac medal winner in India, many Fellows of the Royal Society and five Nobel laureates as of 2019 which is highest in South Asia.

University Of Calcutta

Inflammation

Alarming increase of death due to S. aureus sepsis demands newer treatment strategies. Enhancement of antibiotic resistant S. aureus strains caused increased mortality. Only antibiotic treatment for Staphylococcal sepsis has been found insufficient to improve outcomes. In the innate immune response, phagocytosis mediated killing of pathogen and further triggering of intracellular signaling cascades by the PRRs culminates in the release of a variety of pro inflammatory cytokines, which orchestrate together in the early host response to infection. Increased production of inflammatory cytokines not only delineate pathogen burden but also affects host cell by triggering inflammation. Therefore, combinational therapy of Ascorbic acid is used along with antibiotics Ofloxacin (OFX) or Chloramphenicol (CHL) to kill S. aureus by mouse peritoneal macrophages. For this ROS like H2O2, superoxide anion and NO production was accessed, TLR2 and COX2 expression was monitored. Pro-inflammatory cytokines along with antioxidant levels were also analyzed. Ascorbic acid along with antibiotics OFX or CHL promoted bacterial clearance at early infection by increasing H2O2 and O2 −.NO production has been found to decrease, providing protection against harmful per-oxynitril ion. Increase in TLR-2 expression resulted in enhanced phagocytosis and subsequently more killing. Treatment with Ascorbic acid decreased proinflammatory cytokines and inflammatory markers like iNOS and COX2. This combination increased antioxidant enzymes like SOD, Catalase, GSH as well as decreased LPO, thus balancing ROS and antioxidant status inside the cell. Thus in-vitro augmentation of bacterial clearance along with regulated inflammation as found by decrease in proinflammatory cytokines like TNF-α IFN-γ,IL-6 and inflammatory markers like COX2 may be considered as a novel and important therapeutic strategy. © 2017 Elsevier Ltd

Microbial Pathogenesis

Killing of S. aureus in murine peritoneal macrophages by Ascorbic acid along with antibiotics Chloramphenicol or Ofloxacin: Correlation with inflammation

RA associated with oxidative stress and chronic inflammation has been a major health problem among the population worldwide. In this study protective effect of methanolic extract of Adhatoda vasica leaf (AVE) was evaluated on Collagen-induced arthritis in male Swiss albino mice. Post oral administration of AVE at 50, 100 and 200 mg/kg body weight doses decreased the arthritic index and footpad swelling. AVE administration diminished pro-inflammatory cytokines in serum and synovial tissues. Reduced chemokines and neutrophil infiltration in synovial tissues after AVE administration dictated its protective effect against RA. Decreased LPO content and SOD activity along with concomitant rise in GSH and CAT activities from liver, spleen and synovial tissues indicated regulation of oxidative stress by AVE. In addition decreased CRP in serum along with suppressed TLR-2 expression in CIA mice after AVE treatment was also observed. Protective effect of AVE in RA is further supported from histopathological studies which showed improvement during bone damage. In conclusion this study demonstrated A. vasica is capable of regulating oxidative stress during CIA and therefore down regulated local and systemic release of pro-inflammatory mediators, which might be linked to mechanism of decreasing synovial TLR-2 expression via downregulating release of its regular endogenous ligands like CRP. © 2015 The Authors. Published by Elsevier Inc.

Fulltext

Journal of Nutrition and Intermediary Metabolism

Protective effects of methanolic extract of Adhatoda vasica Nees leaf in collagen-induced arthritis by modulation of synovial toll-like receptor-2 expression and release of pro-inflammatory mediators

The administration of melatonin during acute bacterial infection was evaluated in this study. Mice pre-exposed to normal photoperiodic (NP), short photoperiodic (SP), and long photoperiodic (LP) day lengths were infected separately with live Staphylococcus aureus (5 × 106 cells/ml) or Escherichia coli (2.5 × 107 colony-forming units/ml) and treated with melatonin (10 mg/kg body weight). Behavioral studies were performed before bacterial infection and after melatonin administration. In mice pre-exposed to SP, exogenous melatonin administration resulted in better clearance of bacteria from blood and behavioral improvement. Reduced glutathione content and superoxide dismutase activities were increased, with concomitant decrease in lipid peroxidation content and catalase activities in the liver, brain, and spleen after exogenous melatonin administration. The overproduction of tumor necrosis factor-α, interferon-γ, and interleukin-6 during acute bacterial infection in mice exposed to different photoperiods was probably regulated by the administration of exogenous melatonin, by reducing neutrophil recruitment to spleen, expression of inducible nitric oxide synthase and cyclooxygenase-2 in hypothalamus, and C-reactive protein in the serum, and was also associated with improved behavioral response. Photoperiodic variations in inflammatory and oxidative stress markers might be correlated to serum melatonin and corticosterone levels. This study suggests that the administration of melatonin during SP exposure is protective in infection-induced inflammation than NP and LP exposure. © 2016, Springer Science+Business Media New York.

Beneficial Effects of Exogenous Melatonin in Acute Staphylococcus aureus and Escherichia coli Infection-Induced Inflammation and Associated Behavioral Response in Mice After Exposure to Short Photoperiod

Immobilization is an easy and convenient method to induce both psychological and physical stress resulting in restricted motility and aggression and is believed to be the most severe type of stress in rodent models. Although it has been generally accepted that chronic stress often results in immunosuppression while acute stress has been shown to enhance immune responses, the effects of IS on the host resistance to Escherichia coli (E. coli) infection and associated behavioral changes are still not clear. In a series of experiments aimed at determining the level of hypothalamic COX-2, HSP-90, HSP-70, SOD-1 and plasma level of corticosterone, cytokine, antibody titer and their association with behavioral activities, mice were infected with viable E. coli during acute and chronic IS by taping their paws. In this study we show that acute and chronic IS enhances the resistance of mice to E. coli infection via inhibiting the production of pro-inflammatory cytokines, free radicals, and by improving the exploratory behavior. Altogether, our findings support the notion that cytokines released during immune activation and under the influence of corticosterone can modulate the open field behavior both in terms of locomotor activity as well as exploration. One of the features observed with chronic stressor was a lower ability to resist bacterial infection, although in case of acute stress, a better clearance of bacterial infection was observed in vivo with improvement of exploratory behavior and cognitive functions. © 2012 Elsevier Inc.

Brain, Behavior, and Immunity

Increased resistance of immobilized-stressed mice to infection: Correlation with behavioral alterations

To study the effects of gentamicin in combination with ascorbic acid on septic arthritis, mice were infected with Staphylococcus aureus (S. aureus) and treated with gentamicin, which was given at 5 mg/kg after 24 h of infection, followed by ascorbic acid, given at 20 mg/kg body weight after 2 h of gentamicin treatment. Mice were sacrificed at 3, 9, 15 days post-infection (dpi). Combined treatment of infected mice with gentamicin and ascorbic acid eradicated the bacteria from the blood, spleen and synovial tissue and showed a significant gross reduction in arthritis, reduced serum levels of tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). S. aureus-infected mice have demonstrated the disturbed antioxidant status measured in terms of cellular antioxidants like reduced glutathione and antioxidant enzymes such as superoxide dismutase (SOD) and catalase. The same were ameliorated when the animals were co-treated with gentamicin along with ascorbic acid. © 2012 Blackwell Publishing Ltd.

Scandinavian Journal of Immunology

Gentamicin in Combination with Ascorbic Acid Regulates the severity of Staphylococcus aureus Infection-Induced Septic Arthritis in Mice

To determine the interrelationship between the hydrogen peroxide (H2O2) mediated killing and the potential role of bacterial catalase and SOD in the evasion of host defense, we examined three clinical isolates of Staphylococcus aureus and evaluated their intracellular survival mechanism within murine peritoneal macrophages. Fluorescent microscopy and bacterial colony-forming unit (cfu) count revealed that phagocytic capacity of murine peritoneal macrophages was highest after 2 h of in vitro infection with S. aureus. To understand whether catalase and SOD contributing in the intracellular survival, were of bacterial origin or not, 3 amino 1,2,4 triazole (ATZ) and Diethyldithiocarbamic acid (DDC) were used to inhibit specifically macrophage derived catalase and SOD respectively. Catalase activity from the whole staphylococcal cell in presence of ATZ suggested that the released catalase were of extracellular origin. Scanning electron microscopy revealed the degraded host cell membrane integrity during prolonged infection. Purified bacterial catalase from the intracellularly survived S. aureus recovered after 5 h of infection and its inhibition by ATZ in the zymography strengthened the scope of involvement of these anti-oxidants in the intracellular survival of S. aureus. © 2009 Elsevier Ltd. All rights reserved.

Staphylococcal catalase protects intracellularly survived bacteria by destroying H2O2 produced by the murine peritoneal macrophages

Background: Superoxide dismutase (SOD) and catalase are anti-oxidant enzymes potentially used by the bacteria to neutralize macrophage microbicidal molecules such as hydrogen peroxide (H2O2). Objective: To investigate contribution of bacterial anti-oxidant enzymes in intracellular survival of Staphylococcus aureus (S. aureus) within macrophages. Materials: Murine peritoneal macrophages and S. aureus (CMC-524, ICH-629 and ICH-757). Treatment: 106 colony forming units (CFU) of the 90 minutes (min) intracellularly viable S. aureus were administered (i.v.) per mouse through 0.1 ml saline. Methods: Anti-oxidant enzyme assay, phagocytic activity, H 2O2 release, Zymography for catalase, serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) level were estimated. One-way Model I ANOVA and one tail Student's t-test were performed. Results: Survival of S. aureus was least after 90 min of reincubation within macrophages. Maximum amount of bacterial anti-oxidant enzymes were released after 90 min of re-incubation. H2O2 released after 90 min of re-incubation with S. aureus was maximum. Higher activity of catalase and SOD by S. aureus occurred in response to the gradual production of H2O2. Serum IL-6 and TNF-α was also elevated 1h post infection. Conclusions: Bacterial catalase and SOD combat reactive oxygen species enabling S. aureus to persist within macrophages, inducing local inflammation, causing greater induction of serum TNF-α and IL-6. © 2008 Birkhaueser.

Inflammation Research

Intracellular survival of Staphylococcus aureus: Correlating production of catalase and superoxide dismutase with levels of inflammatory cytokines

Neurochemistry International

Understanding the molecular mechanism of blood–brain barrier damage in an experimental model of Japanese encephalitis: Correlation with minocycline administration as a therapeutic agent

Glia

Proinflammatory mediators released by activated microglia induces neuronal death in Japanese encephalitis

Best Practice & Research Clinical Rheumatology

Infectious arthritis

Possible protective role of chloramphenicol in TSST-1 and coagulase-positive Staphylococcus aureus-induced septic arthritis with altered levels of inflammatory mediators

Journal	Data powered by TypesetInflammation
Publisher	Data powered by TypesetSPRINGER/PLENUM PUBLISHERS
ISSN	0360-3997
Open Access	No