Measurement Of Complement Receptor 1 On Neutrophils In Bacterial And Viral Pneumonia

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o Leukocytes lack the complement receptor CR3 due to a defect in CD11 or CD18 peptides and consequently they cannot respond to C3b opsonin. o Alternatively there may a defect in integrin molecules, LFA-1 or mac-1 arising from defective CD11a or CD11b peptides, respectively. o These molecules are involved in diapedesis and

Neutrophil disorders and their management

times of stress, corticosteroids, complement fragments, and catecholamines accelerate the release of mature neutrophils, as well as meta-myelocytes and band cells, into the circulation. Chemotactic substances such as C5a, inter-leukin 8 (IL-8), monocyte chemotactic factor, leukotrienes, and bacterial peptides induce the

BMC Infectious Diseases BioMed Central

Measurement of complement receptor 1 on neutrophils in bacterial and viral pneumonia Ulla Hohenthal1, Jari Nuutila2, Esa-Matti Lilius2, Iina Laitinen2, Jukka Nikoskelainen1 and Pirkko Kotilainen*1 Address: 1Department of Medicine, Turku University Hospital, Kiinamyllynkatu 4 8, 20520 Turku, Finland and 2Department of Biochemistry,

A Neonatal Murine Model of MRSA Pneumonia

innate immune cells results in differences in the adaptive immune response. Evidence suggests that in neonates there is preferential differentiation of naïve CD4+ T cells into Th2 or Th17 subsets

MBL and L-ficolin

CONTENTS Glossary 8 Chapter 1 11 General introduction Chapter 2 49 Coding and non-coding polymorphisms in the lectin pathway activator L-ficolin gene in 188 Dutch blood bank donors Chapter 3 59


measured the receptor expression in various rather small patient groups [4 7]. The summary of the results from these studies is presented in Table 2 In monocytes, all the recep-tors were upregulated in bacterial and viral infections. In neutrophils,CR1,CR3,FcγRI,andFcγRIIwereupregulated, while FcγRIII was downregulated in bacterial


the skin, kidney and joints), activate classical complement pathway and cause inflammatory damage. It is mediated by soluble immune complexes. They are mostly of IgG class, although IgM may also be involved. The reaction takes hours to days (3-10 hours) to develop. The antigen may be exogenous (chronic bacterial, viral or

Iina Laitinen, PhD PhD MSc

Quantitative analysis of complement receptors, CR1 (CD35) and CR3 (CD11b), on neutrophils improves distinction between bacterial and viral infections in febrile patients: Comparison with standard clinical laboratory data. J Immunol Methods. 2006;315(1-2):191-201. 10.

Community-ACquired PneumoniA in Adult PAtients with sPeCiAl

failure or development of complications. The mean expression of complement receptor (CR1) on neutrophils was significantly higher in patients with pneumococcal pneumonia than influenza A pneumonia. Among the 71 BAL samples, only one (1.3%) quantitative bacterial culture was diagnostic for CAP.

FEATURE The Five Fingers of the Diagnostic Evaluation for

activated neutrophils is the test-of-choice for neutrophil function (ie, the neutrophil SIDEBAR The 10 Warning Signs of Primary Immunodeficiency 1. Four or more new ear infections within 1 year. 2. Two or more serious sinus infections within 1 year. 3. Two or more months on antibiotics with little effect. 4. Two or more pneumonias within 1 year. 5.

C-reactive protein

CURB65 ≥3 23.6 97.6 85.2 71.1 Pneumonia severity index ≥3 14.5 99.1 96.3 40.7 Failure of CRP to fall by > 50% on day 4 associated with worse outcomes CURB65 = new onset confusion, urea > 7 mmol/l, RR ≥30/min, SBP < 90 mmHg or DBP ≤60 mmHg, age ≥65 yrs

The use of inflammatory laboratory tests in rheumatology

a quick response by a direct measurement. It reflects the extension of the inflammatory process or clinical activity, especially in bacterial infections (and not viral), hypersensitivity reactions, ischemia and tissue necrosis. Slightly elevated values of CRP can be found in obesity, smoking, diabetes, uremia, hypertension, physical inactivity,


prevalence between 1 in 10,000 and 1 in 100,000. Etiology. A variety of defects in B-cell function or in B cell T cell interaction can produce the clinical picture of common variable immunodeficiency. The genetic basis of this disorder is largely unknown, but a number of genetic defects have recently been elucidated

Primary immunodeficiencies in seriously ill children: Report

providing defenses against viral and bacterial infec-tions. Some types of SCIDs have been defined, based on immunological, genetic and mutation criteria, in 39 distinct genes. The most common defects are mu-tations of the interleukin 2 receptor gamma (IL2RG) gene, Janus kinase 3 gene (JAK3), among others.

Universitatea de Stat de Medicină și Farmacie Nicolae

diffuse (72.1%), focal (12.8%), and mesangial (8.1%) proliferative GN in adults. In postinfectious GN, the glomerulus is hypercellular with marked cellular infiltration (ie, polymorphonuclear neutrophils, monocytes). Immunofluorescence may show fine, granular deposits of immunoglobulin G in a starry sky appearance.