Ques-1: How does silica get into the macrophages? what type of coat do you expect on the vesicles? Answer: Silicosis: Alveolar macrophages have associated with presence of \"surface scavanger receptors-A\" to recognize silica particle and these particles are going to form \"a non-opsonized coat\" on the surface of macrophages and FCR- mediated uptake. This coat formation is completely depends on “the negatively changed ligands of silica particles” & it is carried into the cell via activation of Rac and RhoA GTPases & IP3. This non-opsonized silica uptake into the cell is going to trigger phagosome formation by the lysosomal vesicles to mediate denaturation but failure of cell to denaturate it finally result in lysis of phagolysosomal membranes to leak the internal contents into the cytosplasm Ques-2: The silica particles inside the lysosome to from a endolysosome-to-phagosome fusion finally trigger leakage of internal contents into the cytoplasm of macrophages in alveoli of lung. These events are followed by activation of mitochondria hyperpolarization signaling pathway finally result in \"generation of caspase-9 and -3\" as a result apoptosis or cell death even the patient is not working in the coal mine Solution Ques-1: How does silica get into the macrophages? what type of coat do you expect on the vesicles? Answer: Silicosis: Alveolar macrophages have associated with presence of \"surface scavanger receptors-A\" to recognize silica particle and these particles are going to form \"a non-opsonized coat\" on the surface of macrophages and FCR- mediated uptake. This coat formation is completely depends on “the negatively changed ligands of silica particles” & it is carried into the cell via activation of Rac and RhoA GTPases & IP3. This non-opsonized silica uptake into the cell is going to trigger phagosome formation by the lysosomal vesicles to mediate denaturation but failure of cell to denaturate it finally result in lysis of phagolysosomal membranes to leak the internal contents into the cytosplasm Ques-2: The silica particles inside the lysosome to from a endolysosome-to-phagosome fusion finally trigger leakage of internal contents into the cytoplasm of macrophages in alveoli of lung. These events are followed by activation of mitochondria hyperpolarization signaling pathway finally result in \"generation of caspase-9 and -3\" as a result apoptosis or cell death even the patient is not working in the coal mine.

1. Ques-1: How does silica get into the macrophages? what type of coat do you expect on the
vesicles?
Answer: Silicosis: Alveolar macrophages have associated with presence of "surface scavanger
receptors-A" to recognize silica particle and these particles are going to form "a non-opsonized
coat" on the surface of macrophages and FCR- mediated uptake. This coat formation is
completely depends on “the negatively changed ligands of silica particles” & it is carried into the
cell via activation of Rac and RhoA GTPases & IP3. This non-opsonized silica uptake into the
cell is going to trigger phagosome formation by the lysosomal vesicles to mediate denaturation
but failure of cell to denaturate it finally result in lysis of phagolysosomal membranes to leak the
internal contents into the cytosplasm
Ques-2:
The silica particles inside the lysosome to from a endolysosome-to-phagosome fusion finally
trigger leakage of internal contents into the cytoplasm of macrophages in alveoli of lung. These
events are followed by activation of mitochondria hyperpolarization signaling pathway finally
result in "generation of caspase-9 and -3" as a result apoptosis or cell death even the patient is
not working in the coal mine
Solution
Ques-1: How does silica get into the macrophages? what type of coat do you expect on the
vesicles?
Answer: Silicosis: Alveolar macrophages have associated with presence of "surface scavanger
receptors-A" to recognize silica particle and these particles are going to form "a non-opsonized
coat" on the surface of macrophages and FCR- mediated uptake. This coat formation is
completely depends on “the negatively changed ligands of silica particles” & it is carried into the
cell via activation of Rac and RhoA GTPases & IP3. This non-opsonized silica uptake into the
cell is going to trigger phagosome formation by the lysosomal vesicles to mediate denaturation
but failure of cell to denaturate it finally result in lysis of phagolysosomal membranes to leak the
internal contents into the cytosplasm
Ques-2:
The silica particles inside the lysosome to from a endolysosome-to-phagosome fusion finally
trigger leakage of internal contents into the cytoplasm of macrophages in alveoli of lung. These
events are followed by activation of mitochondria hyperpolarization signaling pathway finally
result in "generation of caspase-9 and -3" as a result apoptosis or cell death even the patient is
not working in the coal mine