Acinetobacter baumannii is the etiologic agent of a wide range of nosocomial infections,including pneumonia, bacteremia, and skin infections. Over the last 45 years, an alarming increase in the antibiotic resistance of this opportunistic microorganism has been reported, a situation that hinders effective treatments. In order to develop effective therapies against A. baumannii it is crucial to understand the basis of host–bacterium interactions, especially those concerning the immune response of the host.

1. ‫هستی‬ ‫خالق‬ ‫یگانه‬ ‫نام‬ ‫به‬
1

3. summary
Acinetobacter baumannii is the etiologic agent of a
wide range of nosocomial infections,including
pneumonia, bacteremia, and skin infections. Over
the last 45 years, an alarming increase in the
antibiotic resistance of this opportunistic
microorganism has been reported, a situation that
hinders effective treatments. In order to develop
effective therapies against A. baumannii it is crucial
to understand the basis of host–bacterium
interactions, especially those concerning the
immune response of the host.
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4. Contents :
Innate immune responses against A.baumannii
0 types of cells
0 soluble factors
0 cytokines & chemokines
Adaptive immune responses against A.baumannii
Tacticts used by acinetobacter to evade host
immunity
Conclusion
refereces
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5. 5
The first line…

6. Types of effector cells in
innate immunity
neutrophil macrophage NK
DC
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7. NEUTROPHILS, ESSENTIAL
PLAYERS
DURING A. baumannii
INFECTION
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8. Why neutrophils are so
important ?
observation of high prevalence of infections caused by
Acinetobacter in neutropenic patients.
Evidence of neutrophils limiting different types of A.
baumannii infection including bacteremia, septicemia
and skin infection
8

9. multiple bactericidal
mechanisms by neutrophils :
0 oxidative burst
0 neutrophil extracellular traps (NETs)
9

10. 10

11. bacteria can avoid being
killed by neutrophils
adhere to these cells independently of phagocytic
processes.
dissemination of the bacteria
11

12. macrophages
 alveolar macrophage : an advantage for early
responses
phagocytosis
 production high amounts of MIP-2, IL-6, and TNF-α
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13. Natural killer cells
 Depletion of NKs in a pneumonia model interferes
with bacterial clearance and hence resolution of the
infection.
 The mechanism through which NKs contribute to
control A. baumannii pneumonia is indirect and relies
on the production of the chemoattractant KC, which
in turn recruits neutrophils to the site of infection
13

14. Dendritic cells
 the bridge between innate and adaptive immune
responses
 it become activate in response to A. baumannii LPS
 OmpA activates DCs’ signaling via MAPKs and NFκB
1 )high expression of molecules involved in antigen presentation and
2)production of the inflammatory cytokine IL-12.
 As a consequence, DCs are prone to polarize T cells
into TH1 effectors
14

15. The chemoattractant signals during A.
baumannii infections :
0 Chemokines
0 bacterial metabolites
0 antimicrobial peptides produced by the host
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16. 16
Additional Innate Immune
Effectors in the Immune
Response Against A.
baumannii Infection

17. soluble factors
 antimicrobial peptides
 complement system
17

18. antimicrobial peptides
18
0 e.g : Cathelicidin LL-37
0 the extent of bacterial susceptibility to LL-37 depends
on the presence of (LPS) lps(_):susceptible
 production of antimicrobial peptides in Acinetobacter
baumannii infections interaction of (OmpA) with
TonB

19. Complement system
0 some virulence factors that allow successful evasion
of this defense mechanism :
0 ompA-factor H
0 Biofilm formation : king & collague studying
0 CipA, an outer membrane protein :1)dessimination
2) degradate C3b
0 PKF, a secreted serine protease, could also have a
role in the cleavage of some complement components
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22. ‫منابع‬:
0 1. Qiu H, KuoLee R, Harris G, Chen W. High susceptibility to respiratory Acinetobacter baumannii
infection in A/J mice is associated with a delay in early pulmonary recruitment of neutrophils.
Microbes Infect (2009) 11:946–55. doi:10.1016/j.micinf.2009.06.003
0 2. Bruhn KW, Pantapalangkoor P, Nielsen T, Tan B, Junus J, Hujer KM, et al. Host fate is rapidly
determined by innate effector-microbial interactions during Acinetobacter baumannii bacteremia. J
Infect Dis (2015) 211:1296–305. doi:10.1093/infdis/jiu593
0 3. Breslow JM, Meissler JJ Jr, Hartzell RR, Spence PB, Truant A, Gaughan J, et al. Innate immune
responses to systemic Acinetobacter baumannii infection in mice: neutrophils, but not interleukin-
17, mediate host resistance. Infect Immun (2011) 79:3317–27. doi:10.1128/IAI.00069-11
0 4. Grguric-Smith LM, Lee HH, Gandhi JA, Brennan MB, DeLeon-Rodriguez CM, Coelho C, et al.
Neutropenia exacerbates infection by Acinetobacter baumannii clinical isolates in a murine wound
model. Front Microbiol (2015) 6:1134. doi:10.3389/fmicb.2015.01134
5-Joly-Guillou ML, Wolff M, Pocidalo JJ, Walker F, Carbon C. Use of a new mouse model of Acinetobacter
baumannii pneumonia to evaluate the postantibiotic effect of imipenem. Antimicrob Agents Chemother
(1997) 41:345–51.
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