PMID- 15358650
OWN - NLM
STAT- MEDLINE
DCOM- 20050503
LR  - 20181113
IS  - 1071-412X (Print)
IS  - 1098-6588 (Electronic)
IS  - 1071-412X (Linking)
VI  - 11
IP  - 5
DP  - 2004 Sep
TI  - Increased production of proinflammatory cytokines following infection with 
      porcine reproductive and respiratory syndrome virus and Mycoplasma hyopneumoniae.
PG  - 901-8
AB  - Induction of the proinflammatory cytokines interleukin-1 (IL-1) (alpha and beta), 
      IL-6, IL-8, IL-10, IL-12, and tumor necrosis factor alpha (TNF-alpha) in 
      pulmonary alveolar macrophages (PAMs) was assessed following experimental 
      infection with porcine reproductive and respiratory syndrome virus (PRRSV) and/or 
      Mycoplasma hyopneumoniae by using in vivo and in vitro models. The in vivo model 
      consisted of pigs infected with PRRSV and/or M. hyopneumoniae and necropsied at 
      10, 28, or 42 days postinfection. Pigs infected with both pathogens had a greater 
      percentage of macroscopic lung lesions, increased clinical disease, and slower 
      viral clearance than pigs infected with either pathogen alone. The pigs infected 
      with both PRRSV and M. hyopneumoniae had significantly increased levels of mRNA 
      for many proinflammatory cytokines in PAMs collected by bronchoalveolar lavage 
      (BAL) at all necropsy dates compared to those in uninfected control pigs. 
      Increased levels of IL-1beta, IL-8, IL-10, and TNF-alpha proteins in BAL fluid, 
      as measured by enzyme-linked immunosorbent assay, confirmed the increased 
      cytokine induction induced by the pathogens. An in vitro model consisted of M. 
      hyopneumoniae-inoculated tracheal ring explants cultured with PRRSV-infected 
      PAMs. PAMs were harvested at 6 or 15 h postinfection with either or both 
      pathogens. The in vitro study detected increased IL-10 and IL-12 mRNA levels in 
      PAMs infected with PRRSV at all time periods. In addition, IL-10 protein levels 
      were significantly elevated in the culture supernatants in the presence of M. 
      hyopneumoniae-inoculated tracheal ring explants. The increased production of 
      proinflammatory cytokines in vivo and in vitro associated with concurrent M. 
      hyopneumoniae and PRRSV infection may play a role in the increased rates of 
      pneumonia associated with PRRSV infection. The increased levels of IL-10 may be a 
      possible mechanism that PRRSV and M. hyopneumoniae use to exacerbate the severity 
      and duration of pneumonia induced by PRRSV and modulate the respiratory immune 
      response.
FAU - Thanawongnuwech, Roongroje
AU  - Thanawongnuwech R
AD  - Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames, IA 
      50011, USA.
FAU - Thacker, Brad
AU  - Thacker B
FAU - Halbur, Patrick
AU  - Halbur P
FAU - Thacker, Eileen L
AU  - Thacker EL
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Clin Diagn Lab Immunol
JT  - Clinical and diagnostic laboratory immunology
JID - 9421292
RN  - 0 (Cytokines)
RN  - 0 (Interleukins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cytokines/*biosynthesis
MH  - Inflammation/metabolism
MH  - Interleukins/biosynthesis/genetics
MH  - Macrophages, Alveolar/metabolism/microbiology
MH  - Mycoplasma hyopneumoniae
MH  - Pneumonia/etiology
MH  - Pneumonia of Swine, Mycoplasmal/*immunology
MH  - Porcine Reproductive and Respiratory Syndrome/*immunology
MH  - Porcine respiratory and reproductive syndrome virus
MH  - RNA, Messenger/analysis
MH  - Swine
MH  - Trachea/metabolism/microbiology/pathology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/genetics
PMC - PMC515260
EDAT- 2004/09/11 05:00
MHDA- 2005/05/04 09:00
PMCR- 2004/09/01
CRDT- 2004/09/11 05:00
PHST- 2004/09/11 05:00 [pubmed]
PHST- 2005/05/04 09:00 [medline]
PHST- 2004/09/11 05:00 [entrez]
PHST- 2004/09/01 00:00 [pmc-release]
AID - 11/5/901 [pii]
AID - 0013-04 [pii]
AID - 10.1128/CDLI.11.5.901-908.2004 [doi]
PST - ppublish
SO  - Clin Diagn Lab Immunol. 2004 Sep;11(5):901-8. doi: 
      10.1128/CDLI.11.5.901-908.2004.