Anti-inflammatory Cytokines and Cytokine Antagonists

Standiford, Theodore J.

doi:10.2174/1381612003400533

Cited by 60 publications

(40 citation statements)

References 92 publications

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“…TNF-α was significantly increased in E. coli infected group comparing with the control one. This result goes with Theodore [29] who recorded the most marked acute phase reactions in responses to E. coli are the greatest TNF-α responses in blood plasma. This result also agreed with Zimecki et al [30] who reported that I.V.…”

Section: Groups T Protein Gm/dl Albumin Gm/dl α-Globulin Gm/dl β-Glosupporting

confidence: 76%

Studies on the Immunomodulatory Effects of Lactoferrin in Rats Infected with E. coli

El‐Boshy¹,

Abdalla²,

Hassan³

2013

JIBTVA

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Eighty male albino rats of Westar strain (350 ± 10 g), 10 to 12 weeks old were divided into four groups. The groups treated are as following. The first control group (Gp. I) was given intraperitoneally in normal saline (1 mL). The second group (Gp. II) was orally infected with 3 × 10 12 CFU of E. coli /Kg. BW. The third group (Gp. III) was infected with E. coli and treated with (0.5%) lactoferrin (LF) 72 hours before E. coli infection in filtered tap water for the duration of the experiment (21 days). The fourth group (Gp. IV) was administrated with LF only (0.5%) in drinking water. Two separate blood samples were collected from heart puncture at the end of 1 st , and 3 rd week post-treatment for immunological studies. The Leukogram in E. coli treated group was insignificant compared with the control group while lymphocytosis was clear compared with the infected group. Total protein, albumin, α-globulin and β-globulin were insignificantly changed in LF & E. coli treatment group comparing with infected and control groups. TNF-α and γ-globulin are significantly increased in infected group comparing with other treated groups. In conclusion, lactoferrin has powerful antibacterial activity in a variety of ways as well as a safe immunostimulant protein when it is orally administrated.

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Section: Groups T Protein Gm/dl Albumin Gm/dl α-Globulin Gm/dl β-Glosupporting

confidence: 76%

Studies on the Immunomodulatory Effects of Lactoferrin in Rats Infected with E. coli

El‐Boshy¹,

Abdalla²,

Hassan³

2013

JIBTVA

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“…This cytokine is also believed to play an important pathogenic role in type 1 autoimmune diseases (1). Thus, therapeutic modalities based on anti-TNF-α have been developed to treat these conditions (2). On the other hand, TNF-α is also involved in type 1 cell-mediated immune responses to intracellular pathogens such as mycobacteria (3).…”

Section: Introductionmentioning

confidence: 99%

TNF-α is a critical negative regulator of type 1 immune activation during intracellular bacterial infection

Zganiacz

Santosuosso²,

Wang³

et al. 2004

J. Clin. Invest.

170

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TNF-α has long been regarded as a proimmune cytokine involved in antimicrobial type 1 immunity. However, the precise role of TNF-α in antimicrobial type 1 immunity remains poorly understood. We found that TNF-α-deficient (TNF -/-) mice quickly succumbed to respiratory failure following lung infection with replication-competent mycobacteria, because of apoptosis and necrosis of granuloma and lung structure. Tissue destruction was a result of an uncontrolled type 1 immune syndrome characterized by expansion of activated CD4 and CD8 T cells, increased frequency of antigen-specific T cells, and overproduction of IFN-γ and IL-12. Depletion of CD4 and CD8 T cells decreased IFN-γ levels, prevented granuloma and tissue necrosis, and prolonged the survival of TNF -/-hosts. Early reconstitution of TNF-α by gene transfer reduced the frequency of antigen-specific T cells and improved survival. TNF-α controlled type 1 immune activation at least in part by suppressing T cell proliferation, and this suppression involved both TNF receptor p55 and TNF receptor p75. Heightened type 1 immune activation also occurred in TNF -/-mice treated with dead mycobacteria, live replication-deficient mycobacteria, or mycobacterial cell wall components. Our study thus identifies TNF-α as a type 1 immunoregulatory cytokine whose primary role, different from those of other type 1 cytokines, is to keep an otherwise detrimental type 1 immune response in check.

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“…In addition, IL-10 inhibits the surface expression of major histocompatibility complex class II molecules, nitric oxide synthesis, and NF-B nuclear translocation after LPS stimulation and causes the down-regulation of TNF-␣ receptors (16,19,35). Studies have identified IL-10 to be an important regulator of inflammation in a variety of inflammatory disease states, including sepsis (28). For example, increased blood IL-10 levels are found in septic patients, as well as healthy subjects challenged with endotoxin intravenously (21,31).…”

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confidence: 99%

Alveolar Macrophage Deactivation in Murine Septic Peritonitis: Role of Interleukin 10

et al. 2001

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Sepsis predisposes the host to a number of infectious sequelae, particularly the development of nosocomial pneumonia. Mechanisms by which sepsis results in impairment of lung antibacterial host defense have not been well defined. Alveolar macrophages (AM) represent important immune effector cells of the lung airspace. In this study, we examined the effects of cecal ligation and puncture (CLP) on murine AM function ex vivo, including the expression of proinflammatory cytokines and AM phagocytic activity. AM were harvested from mice subjected to a sham operation and CLP 24 h after laparotomy, adherence purified, and challenged with lipopolysaccharide (LPS) or left unstimulated. Both unstimulated and LPS-stimulated AM from mice subjected to CLP (CLP mice) produced significantly smaller amounts of proinflammatory cytokines tumor necrosis factor alpha and interleukin (IL-12) and C-X-C chemokines KC and macrophage inflammatory protein 2 than similarly treated AM from animals subjected to a sham operation. Furthermore, AM isolated from CLP mice displayed a marked impairment in phagocytic activity, as determined by flow cytometry, with this defect persisting to 48 h post-CLP. Induction of peritoneal sepsis syndrome resulted in a time-dependent increase in IL-10 in plasma and peritoneal fluid. Interestingly, the impairment in AM proinflammatorycytokine production and phagocytic activity observed in AM from CLP mice was partially reversed by the in vivo neutralization of IL-10 prior to AM harvest. These observations suggest that abdominal sepsis syndrome results in significant impairment in AM effector cell function, which is mediated, in part, by sepsis-induced expression of IL-10.

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Anti-inflammatory Cytokines and Cytokine Antagonists

Cited by 60 publications

References 92 publications

Studies on the Immunomodulatory Effects of Lactoferrin in Rats Infected with E. coli

Studies on the Immunomodulatory Effects of Lactoferrin in Rats Infected with E. coli

TNF-α is a critical negative regulator of type 1 immune activation during intracellular bacterial infection

Alveolar Macrophage Deactivation in Murine Septic Peritonitis: Role of Interleukin 10

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