III. Histopathological Studies on Cutaneous Reactions to the Bites of Various Arthropods 1

Goldman, Leon; Rockwell, Evelyn; Richfield, Daniel F.

doi:10.4269/ajtmh.1952.1.514

Cited by 39 publications

(20 citation statements)

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“…12,19,[23][24][25][26][27][28][29] Other arthropods capable of producing papular urticaria include mosquitoes and various species of mites. [30][31][32][33][34][35][36][37][38] Histology…”

Section: Etiologymentioning

confidence: 99%

Arthropods in dermatology

Steen

Carbonaro

Schwartz

2004

Journal of the American Academy of Dermatology

171

127

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“…12,19,[23][24][25][26][27][28][29] Other arthropods capable of producing papular urticaria include mosquitoes and various species of mites. [30][31][32][33][34][35][36][37][38] Histology…”

Section: Etiologymentioning

confidence: 99%

Arthropods in dermatology

Steen

Carbonaro

Schwartz

2004

Journal of the American Academy of Dermatology

171

127

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“…Although it is primarily a rodent pathogen, Y. pestis can be transmitted intradermally to humans through the bite of an infected flea (2). It is believed that through this mode of transmission and also aerosol transmission, Y. pestis was responsible for the Black Death in the Middle Ages (3, 4).…”

Section: Introductionmentioning

confidence: 99%

Yersinia pestis Evades TLR4-dependent Induction of IL-12(p40)2 by Dendritic Cells and Subsequent Cell Migration

Robinson

Khader

Locksley

et al. 2008

The Journal of Immunology

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At the temperature of its flea vector (∼20–30°C), the causative agent of plague, Yersinia pestis, expresses a profile of genes distinct from those expressed in a mammalian host (37°C). When dendritic cells (DC) are exposed to Y. pestis grown at 26°C (Y. pestis-26°), they secrete copious amounts of IL-12p40 homodimer (IL-12(p40)2). In contrast, when DCs are exposed to Y. pestis grown at 37°C (Y. pestis-37°), they transcribe very little IL-12p40, which is secreted as IL-12p40 monomer (IL-12p40). Y. pestis-26° also induces migration of DCs to the homeostatic chemokine CCL19, whereas Y. pestis-37° does not; migratory DCs are positive for IL-12p40 transcription and secrete mostly IL-12(p40)2; DCs lacking IL-12p40 do not migrate. Expression of acyltransferase LpxL from Escherichia coli in Y. pestis-37° results in the production of a hexa-acylated lipid A, also seen in Y. pestis-26°, rather than tetra-acylated lipid A normally seen in Y. pestis-37°. The LpxL-expressing Y. pestis-37° promotes DC IL-12(p40)2 production and induction of DC migration. In addition, absence of TLR4 ablates production of IL-12(p40)2 in DC exposed to Y. pestis-26°. The data demonstrate the molecular pathway by which Y. pestis evades induction of early DC activation as measured by migration and IL-12(p40)2 production.

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“…Our results are in line with an early study evaluating skin histopathological changes following Ae. aegypti bites in humans . In this work, skin biopsies at 30 min and 6 hr after mosquito exposure showed a stronger oedema when compared with biopsies after 24 hr, but the cellular infiltrate was more intense at 24 hr than in the initial stages …”

Section: Discussionmentioning

confidence: 48%

“…So far, very few works have characterized in detail the skin inflammatory profile following Ae. aegypti bites over time or in hosts with different immunological history of mosquito exposure . The literature also lacks contemporary approaches to assess this subject.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of inflammatory skin infiltrate following Aedes aegypti bites in sensitized and non‐sensitized mice reveals saliva‐dependent and immune‐dependent phenotypes

et al. 2019

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Summary During probing and blood feeding, haematophagous mosquitoes inoculate a mixture of salivary molecules into their vertebrate hosts’ skin. In addition to the anti‐haemostatic and immunomodulatory activities, mosquito saliva also triggers acute inflammatory reactions, especially in sensitized hosts. Here, we characterize the oedema and the cellular infiltrate following Aedes aegypti mosquito bites in the skin of sensitized and non‐sensitized BALB/c mice by flow cytometry. Ae. aegypti bites induced an increased oedema in the ears of both non‐sensitized and salivary gland extract‐ (SGE‐)sensitized mice, peaking at 6 hr and 24 hr after exposure, respectively. The quantification of the total cell number in the ears revealed that the cellular recruitment was more robust in SGE‐sensitized mice than in non‐sensitized mice, and the histological evaluation confirmed these findings. The immunophenotyping performed by flow cytometry revealed that mosquito bites were able to produce complex changes in cell populations present in the ears of non‐sensitized and SGE‐sensitized mice. When compared with steady‐state ears, the leucocyte populations significantly recruited to the skin after mosquito bites in non‐sensitized and sensitized mice were eosinophils, neutrophils, monocytes, inflammatory monocytes, mast cells, B‐cells and CD4+ T‐cells, each one with its specific kinetics. The changes in the absolute number of cells suggested two cell recruitment profiles: (i) a saliva‐dependent migration; and (ii) a migration dependent on the immune status of the host. These findings suggest that mosquito bites influence the skin microenvironment by inducing differential cell migration, which is dependent on the degree of host sensitization to salivary molecules.

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III. Histopathological Studies on Cutaneous Reactions to the Bites of Various Arthropods 1

Cited by 39 publications

References 0 publications

Arthropods in dermatology

Arthropods in dermatology

Yersinia pestis Evades TLR4-dependent Induction of IL-12(p40)2 by Dendritic Cells and Subsequent Cell Migration

Evaluation of inflammatory skin infiltrate following Aedes aegypti bites in sensitized and non‐sensitized mice reveals saliva‐dependent and immune‐dependent phenotypes

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