			Home About us Contact

Host Inflammatory Response (host + inflammatory_response)

Distribution by Scientific Domains

Medical Sciences	71%

Selected Abstracts

A report from the international consensus on diagnosing and treating the infected diabetic foot,

DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue S1 2004
Benjamin A. Lipsky Chairman
Abstract In persons with diabetes, foot infection, that is, invasion and multiplication of microorganisms in tissues accompanied by tissue destruction or a host inflammatory response, usually begins with skin trauma or ulceration 1. While most foot infections remain superficial, they can spread to subcutaneous tissues, including muscle, joints, and bone. Many diabetic foot ulcers eventuate in an amputation; infection plays a role in approximately 60% of cases 2,4. Neuropathy is the main factor leading to skin breaks, while arterial perfusion largely affects infection outcome. Among the factors predisposing diabetic patients to foot infections are ill-defined immunological perturbations 5, 6; foot anatomy may foster proximal spread of infection and ischemic necrosis 7, 8. Copyright © 2004 John Wiley & Sons, Ltd. [source]

Interferon-, in healthy subjects: selective modulation of inflammatory mediators

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2001
J. De Metz
Background It is suggested that interferon-, (IFN-,), like other cytokines, is a mediator in the host inflammatory response, which could be of importance in the pathophysiology of sepsis. The role of IFN-, in human host inflammatory responses, however, has not been studied. Design In a placebo-controlled trial we studied the acute effects of IFN-, administration on host inflammatory mediators in healthy men: i.e. the cytokine/chemokine cascade system, acute-phase proteins, activation markers of the innate cellular immunity and coagulation/fibrinolysis parameters. Results IFN-, increased plasma levels of interleukin-6 (IL-6), IL-8 and IFN-,-inducible protein-10 (IP-10) (P < 0·05), but did not affect plasma levels of other cytokines (IL-4, IL-10, tumour necrosis factor-,, IL-12p40/p70). Plasma concentrations of C-reactive protein and secretory phospholipase A2 both increased (P < 0·05). Plasma levels of the leucocyte activation marker elastase-,1,antitrypsin complexes increased after IFN-, administration (P < 0·05), IFN-, increased the percentage of high-affinity Fc,-receptor (Fc,RI) -positive neutrophils (P < 0·05), but did not affect the mean fluorescence intensity of Fc,RI on neutrophils. Procoagulant and profibrinolytic effects of IFN-, were evidenced by increased plasma levels of prothrombin fragment F1 + F2, tissue-plasminogen activator and plasmin-,2,antiplasmin complexes (P < 0·05). Conclusion We conclude that IFN-, selectively affects host inflammatory mediators in humans. [source]

Design of Multiresponsive Hydrogel Particles and Assemblies

ADVANCED FUNCTIONAL MATERIALS, Issue 11 2010
Grant R. Hendrickson
Abstract In the realm of soft nanotechnology, hydrogel micro- and nanoparticles represent a versatile class of responsive materials. Over the last decade, our group has investigated the synthesis and physicochemical properties of a variety of synthetic hydrogel particles. From these efforts, several particle types have emerged with potentially enabling features for biological applications, including nanogels for targeted drug delivery, microlenses for biosensing, and coatings for biomedical devices. For example, core/shell nanogels have been used to encapsulate and deliver small interfering RNA to ovarian cancer cells; nanogels used in this fashion may improve therapeutic outcomes for a variety of macromolecular therapeutics. Microgels arranged as multilayers on implantable biomaterials greatly minimize the host inflammatory response to the material. Furthermore, the triggered release of drugs (i.e., insulin) has been demonstrated from similar assemblies. The goal of this feature article is to highlight developments in the design of responsive microgels and nanogels in the context of our recent efforts and in relation to the community that has grown up around this fascinating class of materials. [source]

Gingival crevicular fluid interleukin-1,, prostaglandin E2 and periodontal status in a community population

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2007
Y. Zhong
Abstract Aim: Interleukin-1 , (IL-1,) and prostaglandin E2 (PGE2) are key inflammatory mediators involved in periodontal disease. The purposes of this molecular cross-sectional epidemiological study were to investigate relationships in a community sample between mean concentrations of IL-1, and PGE2 in gingival crevicular fluid (GCF) and (1) clinical periodontal signs and (2) risk factors of host inflammatory response and/or periodontal disease. Material and Methods: The sample comprised 6277 community-dwelling adults aged 52,74 years enrolled in the Atherosclerosis Risk in Communities (ARIC) study. IL-1, and PGE2 concentrations were measured using enzyme-linked immunosorbent assay. Person-level summary variables were computed for maximum pocket depth (MaxPD), maximum clinical attachment level (MaxCAL) and presence/absence of bleeding on probing (BOP). Mean GCF IL-1, and PGE2 concentrations were dependent variables in multiple linear regression models with periodontal measures and covariates as explanatory variables. Results: Both GCF IL-1, and PGE2 were positively related to MaxPD and BOP in multiple regression models (p<0.01). Increased levels of IL-1, and PGE2 were associated with body mass index 30 kg/m2. Conclusion: Higher levels of GCF IL-1, and PGE2 were significantly associated with clinical signs of periodontal disease and independently related to patient-based anthropomorphic measures, behaviours and exposures in community-dwelling adults. [source]

CD4+ CD25+ transforming growth factor-,-producing T cells are present in the lung in murine tuberculosis and may regulate the host inflammatory response,

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007
C. M. Mason
Summary CD4+ CD25+ regulatory T cells produce the anti-inflammatory cytokines transforming growth factor (TGF)-, or interleukin (IL)-10. Regulatory T cells have been recognized to suppress autoimmunity and promote self-tolerance. These cells may also facilitate pathogen persistence by down-regulating the host defence response during infection with Mycobacterium tuberculosis. We evaluated TGF-,+ and IL-10+ lung CD4+ CD25+ T cells in a murine model of M. tuberculosis. BALB/c mice were infected with ,50 colony-forming units of M. tuberculosis H37Rv intratracheally. At serial times post-infection, lung cells were analysed for surface marker expression (CD3, CD4, CD25) and intracellular IL-10, TGF-,, and interferon (IFN)-, production (following stimulation in vitro with anti-CD3 and anti-CD28 antibodies). CD4+ lung lymphocytes were also selected positively after lung digestion, and stimulated in vitro for 48 h with anti-CD3 and anti-CD28 antibodies in the absence and presence of anti-TGF-, antibody, anti-IL-10 antibody or rmTGF-, soluble receptor II/human Fc chimera (TGF,srII). Supernatants were assayed for elicited IFN-, and IL-2. Fluorescence activated cell sorter analyses showed that TGF-,- and IL-10-producing CD4+ CD25+ T cells are present in the lungs of infected mice. Neutralization of TGF-, and IL-10 each resulted in increases in elicited IFN-,, with the greatest effect seen when TGF,srII was used. Elicited IL-2 was not affected significantly by TGF-, neutralization. These results confirm the presence of CD4+ CD25+ TGF-,+ T cells in murine pulmonary tuberculosis, and support the possibility that TGF-, may contribute to down-regulation of the host response. [source]

Interferon-, in healthy subjects: selective modulation of inflammatory mediators

A Salmonella type III secretion effector interacts with the mammalian serine/threonine protein kinase PKN1

CELLULAR MICROBIOLOGY, Issue 5 2006
Andrea Haraga
Summary Essential to salmonellae pathogenesis is an export device called the type III secretion system (TTSS), which mediates the transfer of bacterial effector proteins from the bacterial cell into the host cell cytoplasm. Once inside the host cell, these effectors are then capable of altering a variety of host cellular functions in order to promote bacterial survival and colonization. SspH1 is a Salmonella enterica serovar Typhimurium TTSS effector that localizes to the mammalian nucleus and down-modulates production of proinflammatory cytokines by inhibiting nuclear factor (NF)-,B-dependent gene expression. To identify mammalian binding partners of SspH1 a yeast two-hybrid screen against a human spleen cDNA library was performed. It yielded a serine/threonine protein kinase called protein kinase N 1 (PKN1). The leucine-rich repeat domain of SspH1 was demonstrated to mediate this interaction and also inhibition of NF-,B-dependent gene expression. This suggested that PKN1 may play a role in modulation of the NF-,B signalling pathway. Indeed, we found that expression of constitutively active PKN1 in mammalian cells results in a decrease, while depletion of PKN1 by RNA interference causes an increase in NF-,B-dependent reporter gene expression. These data indicate that SspH1 may inhibit the host's inflammatory response by interacting with PKN1. [source]