Biology Reference
In-Depth Information
diarrheal-causing pathogens or co-infecting GI helminths such as hook-
worm or Trichuris.
The interaction of co-infecting pathogens within the body can be
driven by resource alterations as well as immune-mediated mechanisms.
9
For example, in the gut, Ascaris adult nematodes feed on intestinal
contents and co-infection with diarrhea-causing pathogens may change
the composition or limit the availability of nutrients for Ascaris adult
nematodes. This could lead to stunted nematode growth or fecundity.
10
Immune-mediated mechanisms and alteration in the availability of
resources are not necessarily mutually exclusive considerations in co-
infection biology. When considering Ascaris/HIV co-infection, HIV
multiplies in CD4
Tcells
to become activated or proliferate during Ascaris co-infection may limit
the main resource for HIV viral replication.
In general, magnitude of the interaction between Ascaris co-infection
and an incoming pathogen is likely to be determined by a number of
factors which include the type of infecting pathogen, the organs of the
body infected, the frequency and intensity of infection by Ascaris and
the co-infecting pathogen, the timing and order of the co-infection relative
to Ascaris infection, and the immune responses already present from the
existing Ascaris infection.
Tcells and alterations in the capability of CD4
þ
þ
IMMUNE
RESPONSES TO ASCARIS LUMBR
ICOIDES
To discuss possible immune-mediated interactions between Ascaris and
co-infecting pathogens it is first necessary to review what is known of the
immune responses generated by Ascaris infection (see also Chapter 1). The
generation and maintenance of immune responses during A. lumbricoides
infection has not yet been elucidated in fine detail. However, it is known that
Ascaris is associated with a generic Th2 response typified by the secretion of
IL-4
11
e
13
and circulation of IgE and IgG antibody isotypes to Ascaris
antigens.
14
e
16
The ability of the body to mount Th2 responses is positively
correlated with resistance to this nematode infection.
12,13
Ascaris infection
can also induce a pro-inflammatory immune response. The inflammatory
immune response may benefit one or more stages of the Ascaris life-cycle
because the ability ofmonocytes toproduce the acute phase cytokines tumor
necrosis factor (TNF) and interleukin (IL)-1
b
in response to stimulationwith
Toll-like receptor (TLR) ligands has been positively correlatedwith levels of
fecal Ascaris-egg counts.
17
A pro-inflammatory immune response could
contribute to the maintenance of Ascaris infection by inhibiting the mag-
nitude of the Th2 immune response and associated effector mechanisms.
Ascaris infection is thought to circumvent damaging Th2 effector
mechanisms by the induction of strong immunoregulatory responses in
