Mycobacterium abscessus induces a limited pattern of neutrophil activation that promotes pathogen survival

Autor: Scott D. Sagel, E. Michelle Nichols, Jerry A. Nick, Edward D. Chan, Kenneth C. Malcolm, Milene T. Saavedra, Jennifer L. Taylor-Cousar, Jennifer E. Kret, Lindsay J. Caverly, George M. Solomon, Paul R. Reynolds, Silvia M. Caceres, David P. Nichols, Donna L. Bratton, Stacey L. Martiniano
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Bacterial Diseases
Chemokine
Necrosis
Cystic Fibrosis
Pulmonology
Chronic Obstructive Pulmonary Diseases
Gene Expression
lcsh:Medicine
Mycobacterium abscessus
medicine.disease_cause
Neutrophil Activation
Autosomal Recessive
Superoxides
Molecular Cell Biology
lcsh:Science
Immune Response
0303 health sciences
Multidisciplinary
Innate Immunity
3. Good health
Host-Pathogen Interaction
Infectious Diseases
Staphylococcus aureus
Medicine
Cellular Types
medicine.symptom
Research Article
Immune Cells
Phagocytosis
Immunology
Inflammation
Biology
Microbiology
Mycobacterium
Proinflammatory cytokine
03 medical and health sciences
medicine
Humans
030304 developmental biology
Clinical Genetics
Mycobacterium Infections
030306 microbiology
Gene Expression Profiling
lcsh:R
Immunity
Bacteriology
biology.organism_classification
bacterial infections and mycoses
Emerging Infectious Diseases
Biofilms
Respiratory Infections
biology.protein
bacteria
lcsh:Q
Bacterial Biofilms
Zdroj: PLoS ONE, Vol 8, Iss 2, p e57402 (2013)
PLoS ONE
ISSN: 1932-6203
Popis: Mycobacterium abscessus is a rapidly growing mycobacterium increasingly detected in the neutrophil-rich environment of inflamed tissues, including the cystic fibrosis airway. Studies of the immune reaction to M. abscessus have focused primarily on macrophages and epithelial cells, but little is known regarding the neutrophil response despite the predominantly neutrophillic inflammation typical of these infections. In the current study, human neutrophils released less superoxide anion in response to M. abscessus than to Staphylococcus aureus, a pathogen that shares common sites of infection. Exposure to M. abscessus induced neutrophil-specific chemokine and proinflammatory cytokine genes. Although secretion of these protein products was confirmed, the quantity of cytokines released, and both the number and level of gene induction, was reduced compared to S. aureus. Neutrophils mediated killing of M. abscessus, but phagocytosis was reduced when compared to S. aureus, and extracellular DNA was detected in response to both bacteria, consistent with extracellular trap formation. In addition, M. abscessus did not alter cell death compared to unstimulated cells, while S. aureus enhanced necrosis and inhibited apoptosis. However, neutrophils augment M. abscessus biofilm formation. The response of neutrophils to M. abscessus suggests that the mycobacterium exploits neutrophil-rich settings to promote its survival and that the overall neutrophil response was reduced compared to S. aureus. These studies add to our understanding of M. abscessus virulence and suggest potential targets of therapy.
Databáze: OpenAIRE