PMID- 20976099
OWN - NLM
STAT- MEDLINE
DCOM- 20110224
LR  - 20220309
IS  - 1545-7885 (Electronic)
IS  - 1544-9173 (Print)
IS  - 1544-9173 (Linking)
VI  - 8
IP  - 10
DP  - 2010 Oct 19
TI  - Filarial parasites develop faster and reproduce earlier in response to host 
      immune effectors that determine filarial life expectancy.
PG  - e1000525
LID - 10.1371/journal.pbio.1000525 [doi]
LID - e1000525
AB  - Humans and other mammals mount vigorous immune assaults against helminth 
      parasites, yet there are intriguing reports that the immune response can enhance 
      rather than impair parasite development. It has been hypothesized that helminths, 
      like many free-living organisms, should optimize their development and 
      reproduction in response to cues predicting future life expectancy. However, 
      immune-dependent development by helminth parasites has so far eluded such 
      evolutionary explanation. By manipulating various arms of the immune response of 
      experimental hosts, we show that filarial nematodes, the parasites responsible 
      for debilitating diseases in humans like river blindness and elephantiasis, 
      accelerate their development in response to the IL-5 driven eosinophilia they 
      encounter when infecting a host. Consequently they produce microfilariae, their 
      transmission stages, earlier and in greater numbers. Eosinophilia is a primary 
      host determinant of filarial life expectancy, operating both at larval and at 
      late adult stages in anatomically and temporally separate locations, and is 
      implicated in vaccine-mediated protection. Filarial nematodes are therefore able 
      to adjust their reproductive schedules in response to an environmental predictor 
      of their probability of survival, as proposed by evolutionary theory, thereby 
      mitigating the effects of the immune attack to which helminths are most 
      susceptible. Enhancing protective immunity against filarial nematodes, for 
      example through vaccination, may be less effective at reducing transmission than 
      would be expected and may, at worst, lead to increased transmission and, hence, 
      pathology.
FAU - Babayan, Simon A
AU  - Babayan SA
AD  - Centre for Immunity, Infection and Evolution, University of Edinburgh, Edinburgh, 
      United Kingdom. s.babayan@ed.ac.uk
FAU - Read, Andrew F
AU  - Read AF
FAU - Lawrence, Rachel A
AU  - Lawrence RA
FAU - Bain, Odile
AU  - Bain O
FAU - Allen, Judith E
AU  - Allen JE
LA  - eng
GR  - BB/D013550/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - BB/F011180/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
GR  - G0600818/MRC_/Medical Research Council/United Kingdom
GR  - WT_/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20101019
PL  - United States
TA  - PLoS Biol
JT  - PLoS biology
JID - 101183755
RN  - 0 (Interleukin-5)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
CIN - PLoS Biol. 8:e1000524.
MH  - Adaptive Immunity/*physiology
MH  - Animals
MH  - Eosinophils/immunology
MH  - *Filarioidea/growth & development/immunology/parasitology
MH  - Humans
MH  - Interleukin-4/immunology
MH  - Interleukin-5/immunology
MH  - Life Cycle Stages/physiology
MH  - *Life Expectancy
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Reproduction/*physiology
PMC - PMC2957396
COIS- The authors have declared that no competing interests exist.
EDAT- 2010/10/27 06:00
MHDA- 2011/02/25 06:00
PMCR- 2010/10/19
CRDT- 2010/10/27 06:00
PHST- 2009/09/22 00:00 [received]
PHST- 2010/09/07 00:00 [accepted]
PHST- 2010/10/27 06:00 [entrez]
PHST- 2010/10/27 06:00 [pubmed]
PHST- 2011/02/25 06:00 [medline]
PHST- 2010/10/19 00:00 [pmc-release]
AID - 09-PLBI-RA-4135R4 [pii]
AID - 10.1371/journal.pbio.1000525 [doi]
PST - epublish
SO  - PLoS Biol. 2010 Oct 19;8(10):e1000525. doi: 10.1371/journal.pbio.1000525.