Transcript lecture_28_March 19_EPN

Immune Response of Insects
Presence of Pathogens
Recognition?
communication
Hemocytes?
Fat body
Molecules of
Molecules of
communicacion
Serine
Proteases
?
Hemocytes
Transferrin
Activation via Toll,
IMD, y IRD
ProPO
Serine
Proteases
Tyrosine
Production of
Immune peptides
PO
DDC
DCE
Melanotic encapsulation
Phagocytosis
Antimicrobial compounds
Defensins
Cecropins
Proline-Rich Peptides
Glycine-Rich Peptides
Others?
Antimicrobial
Activity
Rhodnius prolixus
T. Cruzi
Anopheles gambiae
P. falciparum
All of this is based on the concept that the parasite/pathogen can get
into a host.
In vectors- enter with a bloodmeal from an infected vertebrate.
How else can parasites/pathogens get in?
What do you do if you want to get into a host, but when you do you are killed.
Who can you enlist to help you?
In the colonization process: “the enemy of my enemy is my friend”.
Who could you ask for help?
1) others of your same species
2) others from different, but related species?
3) other distantly related species?
What about parasitoids?
What about other potential lethal
parasites?
Why are these invaders not killed by components of the innate immune response?
Lepidopteran larvae-caterpillars
Nematode parasites enter but are killed by components of the innate immune
response of the insects.
Bacteria cannot get into the larvae with any predictability
Nematode + bacteria= potent pathogenic duo.
Nematode-Bacterium Complex
Entomopathogenic nematodes
Nematode-bacterium specificity
Lepidopteran host specificity
The entomopathogenic nematodes from the genus Heterorhabditis and
Steinernema have entered a symbiotic relationship with bacteria,
apparently independent from one another.
These bacteria belong to the Enterobacteriaceae, and are closely related
to Escherichia coli, our intestinal bacteria, yet they are not harmful to man
as they do not grow at temperatures above 35°C.
These symbiotic nematodes are able to kill the infected insects fast.
Other related species with no symbiotic bacteria penetrate the insect
larvae, but they have to wait until the insect dies. Yet other species only
attack dead insects.
Due to the symbiosis, entomopathogenic nematodes can use the living
insect as an energy resource, and the symbiotic bacteria who would not
enter body cavity of the insect without the nematodes.
Once in the insect's blood system the nematodes release the bacteria who
proliferate fast and kill the insect in approximately 3 days. The bacteria and the
insect tissue digested by them forms the food supply for the proliferating
nematodes. The proliferation inside an insect can be several 100-thousand fold.
Steinernema sp.-----Xenorhabdus sp.
Heterorhabditis sp. ----- Photorhabdus sp.
Fig. 2. Location of symbiotic bacteria in intestines of their respective
nematode hosts. (A) Xenorhabdus nematophila cells located in the
intestinal vesicle of Steinernema carpocapsae infective juveniles
(magnification approximately 1/2 that B). (B) Photorhabdus luminescens
cells located in the anteriors and mid-intestine of Heterorhabditis
bacteriophora nematodes. In both panels, the images are overlays of
epifluorescent and light (Nomarski in B) micrographs. The bacteria are
fluorescent due to heterologous expression of the green fluorescent
protein (GFP). The bacteria are denoted by arrows and the anteriors of the
nematodes are to the top of the figure.
The nematode then feeds on the reproducing bacteria. Commercial
products contain the infective juvenile stage of various species. Each
species and strain of nematode seems to be most active against a
rather narrow groups of insects.
Bio-insecticide products based on entomopathogenic nematodes
consist of the infective juveniles stage of the EPN life cycle. Infective
juveniles can survive in moist soil for extended periods of time, but do
not feed, surviving on stored energy reserves until a host is located.
The infective juveniles invade the host, via natural body openings
(mouth, anus, spiracles).
They penetrate the hemocoel. The infective juveniles release the
bacterium into the hemolymph. The bacteria rapidly multiply and the
toxins produced kill the insect by septicemia. The nematodes feed upon
the bacteria and degraded insect tissue and develop to first generation
adult males and females, 2-3 generations.
As the insect resource becomes exhausted, most of the juveniles
differentiate into third stage juveniles, to become the survival form of
the life cycle. The insect cuticle then ruptures and the third stage
ensheathed juveniles escape into the surrounding environment.
Caterpillar-nematode-bacterium
Inject E. coli into caterpillar-
immune response- bacteria killed.
Inject M. luteus into caterpillar-
immune response, bacteria killed.
Inject nematode into caterpillar-
nematode killed.
Inject associated bacterium into caterpillar-
caterpillar killed
Parasitoids
The Campoletis sonorensis polydnavirus replicates and is assembled only in the
calyx cells of the female oviducts. CsPDV is injected along with the egg and venom
at the time of oviposition into the larval host. CsPDV disables the normally vigorous
cellular and humoral responses against the egg. After hatching, the endoparasitic
wasp larvae develops within the hemocoel of the lepidopteran host, before
emerging to spin a cocoon and pupate.
Melanotic encapsulation
(A) CsPDV effects upon the defensive melanization pathway. (B) CsPDV effects
upon the cell-mediated encapsulation response. Encapsulation includes recruitment
of plasmatocytes, capsule formation and granulocyte mediated capsule completion.
(C) CsPDV effect upon the induction of antibacterial proteins from the fat body and
hemocytes. Hatched bars represent points in the three response pathways inhibited
by CsPDV. Abbreviations: NADA, N-acetyl dopamine; DT, dopachrome
tautomerase; DDC, DOPA decarboxylase; PO, phenoloxidase; DAT, dopamine
acetyl transferase; QMI, quinone methide isomerase; QI, quinone isomerase; ROS,
reactive oxygen species; Rel X, rel-like transcription factor.
Polydnaviruses are symbiotic proviruses of some ichneumonid and braconid
wasps that modify the physiology, growth and development of host lepidopteran
larvae.
Polydnavirus infection targets neuroendocrine and immune systems, altering
behavior, stunting growth, and immobilizing immune responses to wasp eggs
and larvae. Polydnavirus-mediated disruption of cellular and humoral immunity
renders parasitized lepidopteran larvae suitable for development of wasp larvae
as well as more susceptible to opportunistic infections.
Evidence from the Campoletis sonorensis polydnavirus system indicates that
the unique genomic organization of polydnaviruses may have evolved to
amplify the synthesis of immunosuppressive viral proteins. Immunosuppressive
viruses have been essential to elucidating vertebrate immunity. Polydnaviruses
have similar potential to clarify insect immune responses and may also provide
novel insights into the role of insect immunity in shaping polydnavirus
genomes.
The capacity of virulent strains of
the endoparasitoid L. boulardi to
circumvent melanotic
encapsulation is attributed to
parasitoid-derived ISFs
introduced into host larvae of D.
melanogaster. ISFs may target
one or more elements of the
cellular immune cascade,
including melanogenesis, which
involves Toll pathway regulation of
Spn27A.
Some organisms have formed alliances with unrelated
organisms in a mutualistic relationship to allow for a
combination that allows a parasite relationship to exist.
How did this evolve?
Coevolution ???