This can be identified as a splice site mutation because:

• It is not within the exon (coding region) so it cannot be a missense or nonsense mutation
• Missense is the coding of the wrong amino acid
• Nonsense is the premature insertion of a stop codon
• It is occurring in the intron, and since the majority of splice sites are GT-AG, this causes an alternative splice site (see here)
• Mutations are by definition an error that has been permanently incorporated into the DNA and thus the progeny of the cell so they are unlikely to interfere with replication (though mutations in the promotor region might interfere with transcription)
• Polyadenylation occurs after translation and mutations (unless they are in the proteins responsible for polyadenylation) are unlikely to interfere with polyadenylation. PolyA polymerase does not require a transcript

Eukaryotic mRNA processing = FA2020 p41

Even without knowing the splice site mutation code, the answer can be inferred from elimination.

The basics of this question are what are the major chemotactic factors that attract neutrophils to the site of injury.

These are: IL-8, C5a, LTB4, kallikrein, and platelet activating factor

FA2020 p406 and 215

Important cytokines are on p108