PMID- 10583590
OWN - NLM
STAT- MEDLINE
DCOM- 20000104
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 98
IP  - 3
DP  - 1999 Nov
TI  - Systemic mycobacterial infection inhibits antigen-specific immunoglobulin E 
      production, bronchial mucus production and eosinophilic inflammation induced by 
      allergen.
PG  - 329-37
AB  - As the burden of infectious diseases becomes reduced in many countries, a 
      remarkable increase in the incidence of allergies has occurred. The basis for the 
      rise in atopic disorders as a correlate of the decline in infectious diseases has 
      not been defined. In the present study, we tested experimentally whether prior 
      systemic infection with Mycobacterium bovis bacillus Calmette Guerin (BCG) had 
      any effect on ovalbumin (OVA) Al(OH)3 (alum)-induced immunoglobulin E (IgE) 
      production, airway mucus production and eosinophilic inflammation. The data 
      showed that allergen-specific IgE production and OVA-induced eosinophilia and 
      goblet cell development were significantly inhibited by prior infection with BCG. 
      Correspondingly, following immunization with OVA alum, BCG-infected mice 
      exhibited significantly higher levels of allergen-driven interferon-gamma 
      (IFN-gamma) production than the mice without infection. The ratio of IFN-gamma: 
      interleukin (IL)-4 production was higher in OVA-sensitized mice with prior BCG 
      infection than in those without infection. The abrogation of OVA-induced mucus 
      production and pulmonary eosinophilia in BCG-infected mice correlated with 
      significantly decreased IL-5 production and increased IFN-gamma and IL-12 
      production. These data provide direct evidence that intracellular bacterial 
      infection (i.e. BCG) can inhibit antigen-specific IgE and airway reactivity 
      induced by environmental allergen. Furthermore, the results suggest that changes 
      in cytokine-producing patterns of T lymphocytes and other cells may be the 
      mechanism by which infections influence allergies.
FAU - Yang, X
AU  - Yang X
AD  - Immune Regulation of Allergy Research Group, Laboratory for Infection and 
      Immunity, Department of Medical Microbiology, Faculty of Medicine, University of 
      Manitoba, Winnipeg, Manitoba, Canada.
FAU - Wang, S
AU  - Wang S
FAU - Fan, Y
AU  - Fan Y
FAU - Zhu, L
AU  - Zhu L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Allergens)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Interleukin-5)
RN  - 187348-17-0 (Interleukin-12)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 9006-59-1 (Ovalbumin)
SB  - IM
MH  - Allergens/immunology
MH  - Animals
MH  - Bronchi/immunology/*metabolism
MH  - Female
MH  - Goblet Cells/immunology
MH  - Immunoglobulin E/*blood
MH  - Immunoglobulin G/metabolism
MH  - Interferon-gamma/metabolism
MH  - Interleukin-12/metabolism
MH  - Interleukin-4/metabolism
MH  - Interleukin-5/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mucus/*metabolism
MH  - *Mycobacterium bovis
MH  - Ovalbumin/immunology
MH  - Pulmonary Eosinophilia/*immunology/microbiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tuberculosis/*immunology
PMC - PMC2326954
EDAT- 1999/12/03 00:00
MHDA- 1999/12/03 00:01
PMCR- 2000/11/01
CRDT- 1999/12/03 00:00
PHST- 1999/12/03 00:00 [pubmed]
PHST- 1999/12/03 00:01 [medline]
PHST- 1999/12/03 00:00 [entrez]
PHST- 2000/11/01 00:00 [pmc-release]
AID - imm856 [pii]
AID - 10.1046/j.1365-2567.1999.00856.x [doi]
PST - ppublish
SO  - Immunology. 1999 Nov;98(3):329-37. doi: 10.1046/j.1365-2567.1999.00856.x.