Mast cells in Wallerian degeneration: Morphologic and ultrastructural changes

Esposito, B; Santis, A. De; Monteforte, Rossella; Baccari, Gabriella Chieffi

doi:10.1002/cne.10169

Cited by 20 publications

(10 citation statements)

References 74 publications

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“…Only sporadically were some immature MC observed adhering to the blood capillaries within the brain parenchyma where they were never observed in association with neurons. Some of the MC were metachromatic with Toluidine blue and safraninpositive with AB/safranin, which indicated that the MC were mature cells as earlier described for the MC in other frog tissues (see Chieffi Baccari et al, 1998;Chieffi Baccari et al, 2003;Esposito et al, 2002). Intraperitoneal administration of T 3 and T 4 accelerates larval development; just one week after T 3 -and T 4 -injections the premetamorphic tadpoles had reached the advanced pro-metamorphic stage overlapping with the beginning of climax (stages 30-31).…”

Section: Effects Of Ptu T 3 and T 4 Treatment On Brain MC Populationsupporting

confidence: 70%

Mast cell population in the frog brain: distribution and influence of thyroid status

Monteforte

Pinelli

Santillo

et al. 2010

Journal of Experimental Biology

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SUMMARYIn the developing frog brain, the majority of mast cells (MC) are distributed in the pia mater, and some immature MC are located adjacent to the blood capillaries in and around the neuropil. In the adult brain, MC are more numerous than in pre-and prometamorphic tadpoles; they are mainly located within the pia mater and are particularly numerous in the choroid plexuses. Many MC are found within the brain ventricles juxtaposed to the ependymal lining. MC are rarely observed in the brain parenchyma. In the adult brain, MC number is much higher than in the brain of post-metamorphic froglets. In the latter, MC number is nearly 2-fold over that found in the pre-metamorphic brain. Treatment of pre-and pro-metamorphic tadpoles with 3,5,3Ј-triiodothyronine (T 3 ) and thyroxine (T 4 ) stimulates overall larval development but does not induce a significant change in MC population within the brain. By contrast, treatment with 6-n-propyl-2-thiouracil (PTU) delays larval development and leads to a significant numerical increase of brain MC. In the adult, PTU treatment also has a similar effect whereas hypophysectomy causes a drastic decrease of MC population. The negative effects of hypophysectomy are successfully counteracted by a two-week replacement therapy with homologous pars distalis homogenate. In the adult frog, MC population seems to be refractory to thyroid hormone treatment. The present study on frog brain suggests that pituitary-thyroid axis may be involved in the regulation of MC frequency.

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Section: Effects Of Ptu T 3 and T 4 Treatment On Brain MC Populationsupporting

confidence: 70%

Mast cell population in the frog brain: distribution and influence of thyroid status

Monteforte

Pinelli

Santillo

et al. 2010

Journal of Experimental Biology

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“…Therefore, nerve growth factor might play an important role in both perineurial and mast cell differentiation. This hypothesis is supported by the observation that the Wallerian degeneration, during which a proliferation of both perineurial and mast cells has been shown (Esposito et al, 2002;Latker et al, 1991;Olsson, 1968;Olsson and Sjostrand, 1969), is also characterized by an increase of NGF synthesis (Heumann et al, 1987). In addition, similarly to nerve cells, both mast cells (Nilsson et al, 1997;Otten et al, 1994;Tam et al, 1997) and perineurial cells synthesize and express NGF-receptors TrkA (Bronzetti et al, 1995;Ribeiro-daSilva et al, 1991;Yamamoto et al, 1992).…”

Section: Mast Cell-nerve Interactionsmentioning

confidence: 78%

Induced maturation of frog mast cells by nerve growth factor during ontogenesis

Baccari

Raucci

Fiore

et al. 2003

Microscopy Res & Technique

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The effect of nerve growth factor (NGF) on ontogenesis of frog mast cells was investigated in vivo by histochemical, morphometric, and ultrastructural analysis. Three groups of tadpoles at various stages of development were used. In the first group, the larvae received i.p. injections of 1 ng NGF/g; the second group received 10 ng NGF/g, while the control group received only the vehicle. The first recognizable mast cells arose symmetrically in the tongue at stage 26 of Witschi's standard table. At stages 26 and 29, the mast cell number in the NGF-injected tadpoles was significantly higher than the control group. From stage 29 onward, the mast cell number rapidly increased in all groups. No significant differences in mast cell number were observed between the control group and the NGF-injected groups at stages 31 and 33. Electron microscopy revealed that at metamorphic climax (stage 33), the mast cells in the NGF-treated groups were more mature than those in the control group. Therefore, nerve growth factor at early stages of tadpole development is likely to induce differentiation of mast cell precursors, while at later stages it is likely to induce maturation of immature mast cells. The close anatomical association between mast cells and perineurium, observed during nerve development, is intriguing. Already in the early stages of nerve development, the mast cells form a network around Schwann cell-axon complexes, together with the perineurial cells. At climax, the mast cells are located between the perineurial layers, suggesting that they may play a role in the tissue-nerve barrier of the perineurium. Nerve growth factor also seems to induce perineurial cell maturation.

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“…In turn, recruited macrophages become a source of secreted cytokine and trophic factor release, inducing a complex inflammatory cascade (Stratton et al, ; Tomlinson, Zygelyte, Grenier, Edwards, & Cheetham, ). Mast cells are also recruited (Esposito, De Santis, Monteforte, & Baccari, ), orchestrating complex vascular and immune cell responses, including the chemoattraction of phagocytic neutrophils that further contribute to myelin clearance (Lindborg et al, ). In comparison, ALS nerve pathology similarly involves reactive changes in SCs (Keller, Gravel, & Kriz, ) as well as the recruitment of monocytes, macrophages, mast cells, and neutrophils (Chiu et al, ; Trias et al, ; Van Dyke et al, ).Such immune cell infiltration of the peripheral motor pathways in ALS has been linked to both protective and deleterious effects on motor neuron degeneration and disease progression (Nardo et al, ).…”

Section: Introductionmentioning

confidence: 99%

Schwann cells orchestrate peripheral nerve inflammation through the expression of CSF1, IL‐34, and SCF in amyotrophic lateral sclerosis

Trías

Kovacs

King

et al. 2019

Glia

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Distal axonopathy is a recognized pathological feature of amyotrophic lateral sclerosis (ALS). In the peripheral nerves of ALS patients, motor axon loss elicits a Wallerian‐like degeneration characterized by denervated Schwann cells (SCs) together with immune cell infiltration. However, the pathogenic significance of denervated SCs accumulating following impaired axonal growth in ALS remains unclear. Here, we analyze SC phenotypes in sciatic nerves of ALS patients and paralytic SOD1G93A rats, and identify remarkably similar and specific reactive SC phenotypes based on the pattern of S100β, GFAP, isolectin and/or p75NTR immunoreactivity. Different subsets of reactive SCs expressed colony‐stimulating factor‐1 (CSF1) and Interleukin‐34 (IL‐34) and closely interacted with numerous endoneurial CSF‐1R‐expressing monocyte/macrophages, suggesting a paracrine mechanism of myeloid cell expansion and activation. SCs bearing phagocytic phenotypes as well as endoneurial macrophages expressed stem cell factor (SCF), a trophic factor that attracts and activates mast cells through the c‐Kit receptor. Notably, a subpopulation of Ki67+ SCs expressed c‐Kit in the sciatic nerves of SOD1G93A rats, suggesting a signaling pathway that fuels SC proliferation in ALS. c‐Kit+ mast cells were also abundant in the sciatic nerve from ALS donors but not in controls. Pharmacological inhibition of CSF‐1R and c‐Kit with masitinib in SOD1G93A rats potently reduced SC reactivity and immune cell infiltration in the sciatic nerve and ventral roots, suggesting a mechanism by which the drug ameliorates peripheral nerve pathology. These findings provide strong evidence for a previously unknown inflammatory mechanism triggered by SCs in ALS peripheral nerves that has broad application in developing novel therapies.

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Mast cells in Wallerian degeneration: Morphologic and ultrastructural changes

Cited by 20 publications

References 74 publications

Mast cell population in the frog brain: distribution and influence of thyroid status

Mast cell population in the frog brain: distribution and influence of thyroid status

Induced maturation of frog mast cells by nerve growth factor during ontogenesis

Schwann cells orchestrate peripheral nerve inflammation through the expression of CSF1, IL‐34, and SCF in amyotrophic lateral sclerosis

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