Profiling infection responses in the haemocytes of the mosquito, Aedes aegypti

Mayhew, George F.; Fuchs, Jeremy F.; Rocheleau, Thomas A.; Erickson, Sara M.; Aliota, Matthew T.; Christensen, Bruce M.

doi:10.1111/j.1365-2583.2007.00773.x

Cited by 36 publications

(30 citation statements)

References 76 publications

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“…In A. aegypti , for example, bacterial infection of the hemocoel elicits a phagocytic response by hemocytes followed by inducible expression of antimicrobial peptides [13], [21], while entry into the hemocoel from the gut by filarial nematodes activates cellular and melanotic defenses [34]. In the malaria vector Anopheles gambiae , passage of Plasmodium to the hemolymph-bathed basal side of the midgut exposes the parasite to complement-like thioester-containing proteins from hemocytes that contribute to parasite killing [18].…”

Section: Discussionmentioning

confidence: 99%

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti

2011

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All vector mosquito species must feed on the blood of a vertebrate host to produce eggs. Multiple cycles of blood feeding also promote frequent contacts with hosts, which enhance the risk of exposure to infectious agents and disease transmission. Blood feeding triggers the release of insulin-like peptides (ILPs) from the brain of the mosquito Aedes aegypti, which regulate blood meal digestion and egg formation. In turn, hemocytes serve as the most important constitutive defense in mosquitoes against pathogens that enter the hemocoel. Prior studies indicated that blood feeding stimulates hemocytes to increase in abundance, but how this increase in abundance is regulated is unknown. Here, we determined that phagocytic granulocytes and oenocytoids express the A. aegypti insulin receptor (AaMIR). We then showed that: 1) decapitation of mosquitoes after blood feeding inhibited hemocyte proliferation, 2) a single dose of insulin-like peptide 3 (ILP3) sufficient to stimulate egg production rescued proliferation, and 3) knockdown of the AaMIR inhibited ILP3 rescue activity. Infection studies indicated that increased hemocyte abundance enhanced clearance of the bacterium Escherichia coli at lower levels of infection. Surprisingly, however, non-blood fed females better survived intermediate and high levels of E. coli infection than blood fed females. Taken together, our results reveal a previously unrecognized role for the insulin signaling pathway in regulating hemocyte proliferation. Our results also indicate that blood feeding enhances resistance to E. coli at lower levels of infection but reduces tolerance at higher levels of infection.

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Section: Discussionmentioning

confidence: 99%

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti

2011

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“…Hemocytes are important immune effector cells that are thought to participate in pathogen recognition, mediate fat body production of immune peptides and mediate and coordinate the mosquito systemic immune response [1–3]. Recently, hemocyte differentiation has been also shown to play an important role in innate immune memory responses in A. gambiae mosquitoes that enhance the response to subsequent Plasmodium infections [4].…”

Section: Introductionmentioning

confidence: 99%

The Role of Hemocytes in Anopheles gambiae Antiplasmodial Immunity

et al. 2013

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Hemocytes synthesize key components of the mosquito complement-like system, but their role in the activation of antiplasmodial responses has not been established. The effect of activating Toll signaling in hemocytes on Plasmodium survival was investigated by transferring hemocytes or cell-free hemolymph from donor mosquitoes in which the suppressor cactus was silenced. These transfers greatly enhanced antiplasmodial immunity, indicating that hemocytes are active players in the activation of the complement-like system, through an effector/effectors regulated by the Toll pathway. A comparative analysis of hemocyte populations between susceptible G3 and the refractory L3-5 Anopheles gambiae mosquito strains did not reveal significant differences under basal conditions or in response to Plasmodium berghei infection. The response of susceptible mosquitoes to different Plasmodium species revealed similar kinetics following infection with P. berghei,P. yoelii or P. falciparum, but the strength of the priming response was stronger in less compatible mosquito-parasite pairs. The Toll, Imd,STAT or JNK signaling cascades were not essential for the production of the hemocyte differentiation factor (HDF) in response to P. berghei infection, but disruption of Toll, STAT or JNK abolished hemocyte differentiation in response to HDF. We conclude that hemocytes are key mediators of A. gambiae antiplasmodial responses.

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“…Melanization-related enzymes, including PPAE and PAH, were detected in our study, but no other enzymes, such as PPO, PPO-2 (Taft et al, 2001), PPO-3 (Genbank accession number: AF310673), PPO-4 (AF327409), dopa decarboxylase (DDC) (Ferdig et al, 1996), and dopachrome conversion enzyme (DCE) (Johnson et al, 2003) were detected. Similar results also appeared in microarray anaylsis of haemocytes of mosquito, A. aegypti, inoculated with bacteria, in which PAH is the only melanization-related immune gene that responds to the challenge (Bartholomay et al, 2007). In mosquito, no change in transcript abundance of phenoloxidase (PO) was detected in the whole body adult A. aegypti following exposure to bacteria (Taft et al, 2001).…”

Section: Discussionmentioning

confidence: 60%

Gene expression profiling during early response to injury and microbial challenges in the silkworm, Bombyx mori

Liu

Ling

2009

Arch Insect Biochem Physiol

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To identify Bombyx mori genes involved in the early response to injury and microbial challenge, we performed genome-wide gene expression-profiling experiments using oligonucleotide DNA microarrays. Of approximately 23,000 genes examined, 465 displayed changes in mRNA expression levels. Of these, 306 were induced and 159 were repressed in response to injury (injection with phosphate buffer saline) or challenges by Gram-negative (Serratia marcescens), Gram-positive bacteria (Staphylococcus aureus), or fungus (Beauveria bassiana). Many of these differentially expressed genes can be assigned to specific functional groups of the innate immune response, including recognition, signaling, melanization and coagulation, and antimicrobial peptides. Seventeen percent of differentially expressed genes encode proteins with no obvious similarity to known functional domains. Of particular interest is a member of the juvenile hormone-binding protein family, which was highly induced by both injury and microbial challenges. The possible role of juvenile hormone in innate immunity is discussed.

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Profiling infection responses in the haemocytes of the mosquito, Aedes aegypti

Cited by 36 publications

References 76 publications

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti

The Role of Hemocytes in <b><i>Anopheles gambiae</i></b> Antiplasmodial Immunity

Gene expression profiling during early response to injury and microbial challenges in the silkworm, Bombyx mori

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